Publications by authors named "Li-Qun Ren"

31 Publications

Periostin promotes arterial calcification through PPARγ-related glucose metabolism reprogramming.

Am J Physiol Heart Circ Physiol 2021 Apr 9. Epub 2021 Apr 9.

Department of Cardiology, Zhongda Hospital, School of Medicine, Southeast University, Nanjing 210009, P.R., China.

Extracellular matrix (ECM) exerts a list of biological functions, contributing to almost 30% of the osteogenic process. Periostin is a secreted protein that can alter ECM remodeling in response to vascular injury. However, the functional role of periostin in vascular calcification has yet to be fully described. Ex vivo, recombinant periostin accelerated thoracic aortas calcification, increased the expression of glycolysis key enzymes, and disturbed the normal oxidative phosphorylation (OXPHOS), which could be alleviated by the peroxisome proliferation-activated receptor γ (PPARγ) agonist pioglitazone. In vascular smooth muscle cells (VSMCs), recombinant periostin promoted VSMC-osteoblastic phenotype transition and calcium deposition, and suppressed PPARγ expression. Mechanistically, recombinant periostin caused over-activation of glycolysis and mitochondrial dysfunction in VSMCs, as assessed by extracellular acidification rate (ECAR), oxygen consumption rate, and mitochondrial respiratory chain complexes activities. Targeted glycolysis inhibitors reduced mitochondrial calcium overload, apoptosis, and periostin-induced VSMCs calcification. PPARγ agonists preserved glycolysis and OXPHOS in the stimulated microenvironment, and reversed periostin-promoted VSMC calcification. Furthermore, plasma periostin, lactate, and matrix Gla protein levels were measured in 274 patients who underwent computed tomography to determine coronary artery calcium score (Agatston score). Plasma periostin and lactate levels were both linked to an Agatston score of more than zero in patients with coronary artery calcification. There is also a positive correlation between plasma periostin and lactate levels. This study suggests that downregulation of PPARγ is involved in the mechanism by which periostin accelerates arterial calcification, partly through excessive glycolysis activation and unbalanced mitochondrial homeostasis.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1152/ajpheart.01009.2020DOI Listing
April 2021

Icariin attenuates endothelial-mesenchymal transition via H19/miR-148b-3p/ELF5 in ox-LDL-stimulated HUVECs.

Mol Ther Nucleic Acids 2021 Mar 3;23:464-475. Epub 2020 Dec 3.

Department of Experimental Pharmacology and Toxicology, School of Pharmacy, Jilin University, Changchun 130021, Jilin Province, China.

Atherosclerosis is the main cause of cardio-cerebrovascular diseases. Endothelial-mesenchymal transition plays an important role in atherosclerosis. Icariin has a protective effect on atherosclerosis; however, the underlying mechanism remains unclear. In this study, we explored the molecular mechanism underlying the protective function of icariin in oxidized low-density lipoprotein-stimulated human umbilical vein endothelial cells. H19, a long non-coding RNA, was identified to be downregulated in the background of the oxidized low-density lipoprotein-induced endothelial-mesenchymal transition in human umbilical vein endothelial cells. Icariin upregulated H19 expression and inhibited the transformation of endothelial cells into interstitial cells. Overexpression of H19 affected endothelial-mesenchymal transition in oxidized low-density lipoprotein-stimulated human umbilical vein endothelial cells, whereas H19 knockdown reversed endothelial protective effects of icariin and reduced human umbilical vein endothelial cell migration. Knockdown of H19 significantly downregulated oxidized low-density lipoprotein-induced E74-like factor 5 and upregulated miR-148b-3p, which was reversed by icariin. Thus, icariin may play a protective role in atherosclerosis, and H19 may be a potential therapeutic target.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.omtn.2020.11.021DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7809175PMC
March 2021

Luteolin Suppresses the Proliferation of Gastric Cancer Cells and Acts in Synergy with Oxaliplatin.

Biomed Res Int 2020 21;2020:9396512. Epub 2020 Feb 21.

Department of Experimental Pharmacology and Toxicology, School of Pharmaceutical Sciences, Jilin University, Changchun, Jilin, China.

. Gastric cancer, one of the most common malignant tumors worldwide, arises from the gastric mucosal epithelium and severely affects patient health and quality of life. Luteolin (LUT) is a flavonoid found in vegetables and fruits with diverse functions. A large number of studies have confirmed that LUT has an antitumor effect. Therefore, this study is aimed at verifying whether LUT can exert antitumor effects in synergy with oxaliplatin (OXA). As such, we examined the effects of LUT, OXA, and their coadministration in a gastric adenocarcinoma cell line (SGC-7901). We used the MTT assay to quantify the proliferation of SGC-7901 cells, flow cytometry to detect the cell cycle and apoptosis, ELISA to detect the expression of cell-cycle-related proteins, and western blot to detect the expression of related apoptotic factors. The results of this study show that the combination of LUT and OXA inhibited SGC-7901 cell proliferation and induced apoptosis by altering cell-cycle proportions. In addition, the combination also activated Cyt c/caspase signaling in SGC-7901 cells. In summary, LUT synergy with OXA inhibited the proliferation of gastric cancer cells . The present study also elucidated the mechanism by which LUT potentiated the sensitivity of SGC-7901 cells to OXA through the Cyt c/caspase pathway.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1155/2020/9396512DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7057019PMC
December 2020

Protective Effects of Against Pirarubicin-Induced Cardiotoxicity.

Am J Chin Med 2019 17;47(5):1075-1097. Epub 2019 Jul 17.

*Department of Experimental Pharmacology and Toxicology, School of Pharmacy, Jilin University, Changchun 130021, P. R. China.

Pirarubicin (THP) is an anthracycline antibiotic, frequently used for the treatment of various human cancers. Unfortunately, the clinical effectiveness of THP is limited by its dose-related cardiotoxicity. leaf extract is an extract of the dried leaves of L. (a member of the family, AVLE) that has many positive effects on the cardiovascular system and is widely consumed as tea in China. In this study we established a cardiactoxicity rat model, which showed that pretreatment with AVLE attenuated THP-induced myocardial histopathological injury, electrocardiogram abnormalities, and cardiac dysfunction. AVLE also significantly reduced serum levels of malondialdehyde (MDA), brain natriuretic peptide (BNP), creatine kinase (CK-MB), cardiac troponin (CTnT), and lactate dehydrogenase (LDH); and increased serum superoxide dismutase (SOD) levels. Treatment with AVLE or dexrazoxane (DZR) resulted in an increase Cytochrome C (cytc) in the mitochondria and reduced Cytc and cleaved-caspase-3 levels () in cytoplasm. We also found that AVLE significantly reduced voltage-dependent anion channel 1 (VDAC1), adenosine nucleotide transporter 1 (ANT1), and cyclophilin D (CYPD) mRNA expression (). Furthermore, AVLE appeared to exert therapeutic effects in a dose-dependent manner. Our study suggests the anti-oxidant and anti-apoptotic properties of AVLE may be responsible for the observed cardioprotective effects.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1142/S0192415X19500551DOI Listing
January 2020

Clinicopathological parameters predicting recurrence of pT1N0 esophageal squamous cell carcinoma.

World J Gastroenterol 2018 Dec;24(45):5154-5166

Department of Pathology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China.

Aim: To identify the clinicopathological characteristics of pT1N0 esophageal squamous cell carcinoma (ESCC) that are associated with tumor recurrence.

Methods: We reviewed 216 pT1N0 thoracic ESCC cases who underwent esophagectomy and thoracoabdominal two-field lymphadenectomy without preoperative chemoradiotherapy. After excluding those cases with clinical follow-up recorded fewer than 3 mo and those who died within 3 mo of surgery, we included 199 cases in the current analysis. Overall survival and recurrence-free survival were assessed by the Kaplan-Meier method, and clinicopathological characteristics associated with any recurrence or distant recurrence were evaluated using univariate and multivariate Cox proportional hazards models. Early recurrence (≤ 24 mo) and correlated parameters were assessed using univariate and multivariate logistic regression models.

Results: Forty-seven (24%) patients had a recurrence at 3 to 178 (median, 33) mo. The 5-year recurrence-free survival rate was 80.7%. None of 13 asymptomatic cases had a recurrence. Preoperative clinical symptoms, upper thoracic location, ulcerative or intraluminal mass macroscopic tumor type, tumor invasion depth level, basaloid histology, angiolymphatic invasion, tumor thickness, submucosal invasion thickness, diameter of the largest single tongue of invasion, and complete negative aberrant p53 expression were significantly related to tumor recurrence and/or recurrence-free survival. Upper thoracic tumor location, angiolymphatic invasion, and submucosal invasion thickness were independent predictors of tumor recurrence (Hazard ratios = 3.26, 3.42, and 2.06, < 0.001, < 0.001, and = 0.002, respectively), and a nomogram for predicting recurrence-free survival with these three predictors was constructed. Upper thoracic tumor location and angiolymphatic invasion were independent predictors of distant recurrence. Upper thoracic tumor location, angiolymphatic invasion, submucosal invasion thickness, and diameter of the largest single tongue of invasion were independent predictors of early recurrence.

Conclusion: These results should be useful for designing optimal individual follow-up and therapy for patients with T1N0 ESCC.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3748/wjg.v24.i45.5154DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6288646PMC
December 2018

Heterogenic Distribution of Aromatic L-Amino Acid Decarboxylase Neurons in the Rat Spinal Cord.

Front Integr Neurosci 2017 8;11:31. Epub 2017 Nov 8.

Department of Neuroscience, University of Copenhagen, Copenhagen, Denmark.

Aromatic L-amino acid decarboxylase (AADC) is an essential enzyme in the synthesis of serotonin, dopamine, and certain trace amines and is present in a variety of organs including the brain and spinal cord. It is previously reported that in mammalian spinal cord AADC cells (called D-cells) were largely confined to a region around the central canal and that they do not produce monoamines. To date, there has not been a detailed description of their distribution and morphology in mammals. In the present study this issue is systematically investigated using immunohistochemistry. We have found that AADC cells in the rat spinal cord are both more numerous and more widely distributed than previously reported. In the gray matter, AADC neurons immunolabeled for NeuN were not only found in the region around the central canal but also in the dorsal horn, intermediate zone, and ventral horn. In the white matter a large number of glial cells were AADC-immunopositive in different spinal segments and the vast majority of these cells expressed oligodendrocyte and radial glial phenotypes. Additionally, a small number of AADC neurons labeled for NeuN were found in the white matter along the ventral median fissure. The shapes and sizes of AADC neurons varied according to their location. For example, throughout cervical and lumbar segments AADC neurons in the intermediate zone and ventral horn tended to be rather large and weakly immunolabeled, whereas those in comparable regions of sacrocaudal segments were smaller and more densely immunolabeled. The diverse morphological characteristics of the AADC cells suggests that they could be further divided into several subtypes. These results indicate that AADC cells are heterogeneously distributed in the rat spinal cord and they may exert different functions in different physiological and pathological situations.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3389/fnint.2017.00031DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5706469PMC
November 2017

Cardioprotective effects of rutin in rats exposed to pirarubicin toxicity.

J Asian Nat Prod Res 2018 Apr 27;20(4):361-373. Epub 2017 Oct 27.

a Department of Pharmacology and Toxicology, School of Pharmacy , Jilin University , Changchun 130021 , China.

We established both an acute and chronic cardiac toxicity rat model, which showed pretreatment with rutin attenuated pirarubicin-induced myocardial histopathological injury, electrocardiogram abnormalities, and cardiac dysfunction. Rutin also significantly reduced serum levels of MDA, BNP, CK-MB, CTnT, and LDH and increased serum SOD levels. Treatment with rutin and dexrazoxane resulted in an increase in Bcl-2/Bax ratio (p < 0.05) and reduction in JNK and Caspase-3 protein levels, compared to the pirarubicin group (all p < 0.05). Furthermore, rutin at a dose of 50 mg/kg significantly attenuated the above-mentioned alterations. Our study suggests the antioxidant and anti-apoptotic properties of rutin may be responsible for the cardioprotective effects observed.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1080/10286020.2017.1394292DOI Listing
April 2018

[Effects of icariin on proliferation of vascular smooth muscle cell induced by ox-LDL via impacting MAPK signaling pathway].

Zhongguo Zhong Yao Za Zhi 2016 Oct;41(19):3655-3660

School of Pharmacy, Jilin University, Changchun 130021, China.

This paper was aimed to study the effects of icariin (ICA) on the proliferation of vascular smooth muscle cell (VSMC) induced by oxidized low density lipoprotein (ox-LDL), and the molecular mechanism of the expression of proliferating cell nuclear antigen (PCNA) and MAPK signaling pathway. In this study, VSMC was induced by ox-LDL (50 mg•L⁻¹),the effect of ICA on the proliferation of VSMC was detected by MTT assay, Western blot and Real-time PCR. The results showed that after stimulation of ox-LDL, the proliferation activity of VSMC was increased, S phase, G₂/M phase cells were increased, G₀/G₁ phase cells were decreased, PCNA protein expression was enhanced; ICA (40, 20, 10 μmol•L⁻¹) could effectively inhibit ox-LDL-induced VSMC proliferation, S phase and G₂/M phase cells were decreased, the percentage of cells in G₀/G₁ phase were increased, PCNA expression was decreased, p38MAPK and ERK1/2 activation were inhibited. These results indicate that ICA can inhibit the proliferation of VSMC by reducing the expression of PCNA and blocking the p38MAPK and ERK1/2 signaling pathway.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.4268/cjcmm20161926DOI Listing
October 2016

Anti-hepatocarcinoma activity of TT-1, an analog of melittin, combined with interferon-α via promoting the interaction of NKG2D and MICA.

J Zhejiang Univ Sci B 2017 Jun;18(6):522-531

Department of Experimental Pharmacology and Toxicology, School of Pharmaceutical Sciences, Jilin University, Changchun 130021, China.

Hepatocarcinoma is one of the malignant cancers with significant morbidity and mortality. Immunotherapy has emerged in clinical treatment, owing to the limitation and severe side effects of chemotherapy. In the immune system, natural killer (NK) cells are important effectors required to eliminate malignant tumor cells without the limitation of major histocompatibility complex (MHC) molecule issues. Hence, treatment which could stimulate NK cells is of great interest. Here, we investigated the efficacy of the combined therapy of TT-1 (a mutant of melittin) and interferon-α (IFN-α) on NK cells and human liver cancer HepG-2/Huh7 cells in vitro and in vivo, as well as the mechanism involved. The combination therapy significantly inhibited the growth of HepG-2/Huh7 cells in vivo, but this effect was impaired after depleting NK cells. TT-1 not only up-regulated MHC class I-related chain molecules A (MICA) expression, but also prevented the secretion of soluble MICA (sMICA). Both the mRNA and protein of a disintegrin and metallopeptidase 10 (ADAM 10) in HepG-2/Huh7 cells were decreased after TT-1 treatment. The combined therapy of TT-1 and IFN-α could suppress the growth of HepG-2/Huh7 xenografted tumor effectively via promoting the interaction of NK group 2, member D (NKG2D) and MICA, indicating that TT-1+IFN-α would be a potential approach in treating liver cancer.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1631/jzus.B1600369DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5481301PMC
June 2017

Role of rat autologous skin fibroblasts and mechanism underlying the repair of depressed scars.

Exp Ther Med 2016 Aug 8;12(2):945-950. Epub 2016 Jun 8.

Department of Experimental Pharmacology and Toxicology, Medical School of Jilin University, Changchun, Jilin 130021, P.R. China.

The aim of the present study was to provide reliable experimental evidence for the application of autologous skin fibroblasts (asFbs) in the repair of depressed scars. In the experiments, depressed trauma was induced in male Wistar rats, and fibroblasts were separated from the removed skin tissues to culture in medium. cultured asFbs were injected into the depressed scar sites of rats, and the repair function of asFbs in the depressed scars was then examined at the cellular and whole-animal levels. The expression levels of type I and type III collagen in the dermal layer of the skin injected with asFb cells were significantly higher, as compared with those of the control, and type I collagen expression was significantly higher compared with Type III. Re-injection of asFbs into the dermal layer of depressed scars can markedly improve their repair. These results may prove useful for skin repair in clinical settings.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3892/etm.2016.3442DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4950163PMC
August 2016

Enhanced differentiation of human amniotic fluid-derived stem cells into insulin-producing cells in vitro.

J Diabetes Investig 2017 Jan 30;8(1):34-43. Epub 2016 Jun 30.

Department of Central Laboratory, China-Japan Union Hospital of Jilin University, Changchun, China.

Aims/introduction: To investigate the ability of human amniotic fluid stem cells (hAFSCs) to differentiate into insulin-producing cells.

Materials And Methods: hAFSCs were induced to differentiate into pancreatic cells by a multistep protocol. The expressions of pancreas-related genes and proteins, including pancreatic and duodenal homeobox-1, insulin, and glucose transporter 2, were detected by polymerase chain reaction and immunofluorescence. Insulin secreted from differentiated cells was tested by enzyme-linked immunosorbent assay.

Results: hAFSCs were successfully isolated from amniotic fluid that expressed the pluripotent markers of embryonic stem cells, such as Oct3/4, and mesenchymal stem cells, such as integrin β-1 and ecto-5'-nucleotidase. Here, we first obtained the hAFSCs that expressed pluripotent marker stage-specific embryonic antigen 1. Real-time polymerase chain reaction analysis showed that pancreatic and duodenal homeobox-1, paired box gene 4 and paired box gene 6 were expressed in the early phase of induction, and then stably expressed in the differentiated cells. The pancreas-related genes, such as insulin, glucokinase, glucose transporter 2 and Nkx6.1, were expressed in the differentiated cells. Immunofluorescence showed that these differentiated cells co-expressed insulin, C-peptide, and pancreatic and duodenal homeobox-1. Insulin was released in response to glucose stimulation in a manner similar to that of adult human islets.

Conclusions: The present study showed that hAFSCs, under selective culture conditions, could differentiate into islet-like insulin-producing cells, which might be used as a potential source for transplantation in patients with type 1 diabetes mellitus.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1111/jdi.12544DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5217909PMC
January 2017

Serum B-type natriuretic peptide levels as a marker for anthracycline-induced cardiotoxicity.

Oncol Lett 2016 May 7;11(5):3483-3492. Epub 2016 Apr 7.

Department of Experimental Pharmacology and Toxicology, School of Pharmacy, Jilin University, Changchun, Jilin 130021, P.R. China.

Observational and experimental studies have produced inconsistent evidence about the association of serum levels of B-type natriuretic peptide (BNP) with anthracycline-induced cardiotoxicity (AIC). Therefore, the current meta-analysis examined the association between serum BNP levels and AIC by using data from high quality studies published in peer-reviewed journals. Relevant studies were identified through literature searches of China National Knowledge Infrastructure (CNKI), Web of Science, PubMed, Google Scolar and China BioMedicine (CBM). STATA software was used in this meta-analysis for statistical analysis. In addition, the crude standardized mean difference (SMD) with 95% confidence interval (CI) for the highest vs. the lowest category of serum BNP levels was calculated. A total of 8 independent case-control studies, containing 126 AIC patients and 569 healthy controls, were included for the current meta-analysis. The results indicated a significant difference in serum BNP levels between the cardiotoxic group and normal group, with respect to post-treatment and pretreatment with anthracyclines. Specifically, the serum levels of BNP increased remarkably after treatment with anthracyclines in the cardiotoxic group, compared with the normal group. No publication bias was detected in this meta-analysis. The findings of the present study provide strong evidence that serum BNP levels may be associated with AIC.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3892/ol.2016.4424DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4840927PMC
May 2016

Production of Dopamine by Aromatic l-Amino Acid Decarboxylase Cells after Spinal Cord Injury.

J Neurotrauma 2016 06 30;33(12):1150-60. Epub 2016 Mar 30.

1 Department of Neuroscience and Pharmacology, University of Copenhagen , Copenhagen, Denmark .

Aromatic l-amino acid decarboxylase (AADC) cells are widely distributed in the spinal cord, and their functions are largely unknown. We have previously found that AADC cells in the spinal cord could increase their ability to produce serotonin (5-hydroxytryptamine) from 5-hydroxytryptophan after spinal cord injury (SCI). Because AADC is a common enzyme catalyzing 5-hydroxytryptophan to serotonin and l-3,4-dihydroxyphenylalanine (l-dopa) to dopamine (DA), it seems likely that the ability of AADC cells using l-dopa to synthesize DA is also increased. To prove whether or not this is the case, a similar rat sacral SCI model and a similar experimental paradigm were adopted as that which we had used previously. In the chronic SCI rats (> 45 days), no AADC cells expressed DA if there was no exogenous l-dopa application. However, following administration of a peripheral AADC inhibitor (carbidopa) with or without a monoamine oxidase inhibitor (pargyline) co-application, systemic administration of l-dopa resulted in ∼94% of AADC cells becoming DA-immunopositive in the spinal cord below the lesion, whereas in normal or sham-operated rats none or very few of AADC cells became DA-immunopositive with the same treatment. Using tail electromyography, spontaneous tail muscle activity was increased nearly fivefold over the baseline level. When pretreated with a central AADC inhibitor (NSD-1015), further application of l-dopa failed to increase the motoneuron activity although the expression of DA in the AADC cells was not completely inhibited. These findings demonstrate that AADC cells in the spinal cord below the lesion gain the ability to produce DA from its precursor in response to SCI. This ability also enables the AADC cells to produce 5-HT and trace amines, and likely contributes to the development of hyperexcitability. These results might also be implicated for revealing the pathological mechanisms underlying l-dopa-induced dyskinesia in Parkinson's disease.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1089/neu.2015.4037DOI Listing
June 2016

Spinal cord injury enables aromatic L-amino acid decarboxylase cells to synthesize monoamines.

J Neurosci 2014 Sep;34(36):11984-2000

Department of Neuroscience and Pharmacology, Neuronano Research Center, Department of Experimental Medical Sciences, Lund University, SE-221 00 Lund, Sweden

Serotonin (5-HT), an important modulator of both sensory and motor functions in the mammalian spinal cord, originates mainly in the raphe nuclei of the brainstem. However, following complete transection of the spinal cord, small amounts of 5-HT remain detectable below the lesion. It has been suggested, but not proven, that this residual 5-HT is produced by intraspinal 5-HT neurons. Here, we show by immunohistochemical techniques that cells containing the enzyme aromatic l-amino acid decarboxylase (AADC) occur not only near the central canal, as reported by others, but also in the intermediate zone and dorsal horn of the spinal gray matter. We show that, following complete transection of the rat spinal cord at S2 level, AADC cells distal to the lesion acquire the ability to produce 5-HT from its immediate precursor, 5-hydroxytryptophan. Our results indicate that this phenotypic change in spinal AADC cells is initiated by the loss of descending 5-HT projections due to spinal cord injury (SCI). By in vivo and in vitro electrophysiology, we show that 5-HT produced by AADC cells increases the excitability of spinal motoneurons. The phenotypic change in AADC cells appears to result from a loss of inhibition by descending 5-HT neurons and to be mediated by 5-HT1B receptors expressed by AADC cells. These findings indicate that AADC cells are a potential source of 5-HT at spinal levels below an SCI. The production of 5-HT by AADC cells, together with an upregulation of 5-HT2 receptors, offers a partial explanation of hyperreflexia below a chronic SCI.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1523/JNEUROSCI.3838-13.2014DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6608456PMC
September 2014

Urantide improves atherosclerosis by controlling C-reactive protein, monocyte chemotactic protein-1 and transforming growth factor-β expression in rats.

Exp Ther Med 2014 Jun 31;7(6):1647-1652. Epub 2014 Mar 31.

School of Pharmaceutical Sciences, Jilin University, Changchun, Jilin 130021, P.R. China.

The aim of the present study was to investigate the effects of urantide on the expression status of C-reactive protein (CRP) and the inflammatory cytokines monocyte chemotactic protein (MCP)-1 and transforming growth factor (TGF)-β in the aortas of rats with atherosclerosis (AS), and to identify its underlying mechanisms. The effects of urantide in a rat model of AS and in cultured rat vascular smooth muscle cells (VSMCs) were analyzed via hematoxylin and eosin staining, immunohistochemical staining and ELISA. The results demonstrated that urantide downregulated the expression of inflammatory mediators CRP and MCP-1 and upregulated the expression of TGF-β. The results indicated that urantide inhibited the proliferation of VSMCs. In addition, urantide reduced the expression of CRP and downregulated the secretion of TGF-β in the culture supernatant. In conclusion, urantide ameliorated the arterial inflammatory damage that was observed in the AS rat model at the cell and tissue levels by controlling the expression of CRP and the inflammatory cytokines MCP-1 and TGF-β. Therefore, urantide may be a potential agent for the complementary treatment of AS.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3892/etm.2014.1654DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4043621PMC
June 2014

The urotensin II receptor antagonist, urantide, protects against atherosclerosis in rats.

Exp Ther Med 2013 Jun 9;5(6):1765-1769. Epub 2013 Apr 9.

Department of Pathophysiology, Chengde Medical University, Chengde, Hebei 067000;

The aim of this study was to explore the use of urantide as an antagonist of the urotensin II (UII) receptor, G protein-coupled receptor 14 (GPR14), to protect against atherosclerosis (AS) in rats. The AS rat model was induced by an intraperitoneal injection of vitamin D3 (VD3) into rats fed with a high-fat diet for four weeks. Urantide was then injected into the rats. Immunohistochemical staining, serum biochemical assay, reverse transcription-polymerase chain reaction (RT-PCR) and western blotting were used to investigate the expression of UII and its receptor GPR14 in the AS rat model. Four weeks after induction, pathological changes typical of AS were observed in the AS rat model. In the plaques of the aortic tunica intima and tunica media, expression of UII and GPR14 was observed. The protein and gene expression levels of UII and GPR14 in the model group were significantly increased compared with those in the normal group (P<0.01). Urantide ameliorated the pathological changes of AS in the rat model and reduced the gene and protein expression levels of UII and GPR14 (P<0.05 or P<0.01). UII is associated with AS and the UII receptor GPR14-specific antagonist, urantide, demonstrates the ability to protect against AS. Thus, this study provides new insight and experimental theories for the clinical application of urantide to treat AS.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3892/etm.2013.1052DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3702698PMC
June 2013

Effects of urotensin II and its specific receptor antagonist urantide on rat vascular smooth muscle cells.

Bosn J Basic Med Sci 2013 May;13(2):78-83

Department of Pathophysiology, Chengde Medical College, Chengde 067000, China.

We investigated the effects of urantide, a receptor antagonist of urotensin II (U-II), on the expression of U-II and its receptor GPR14 in rat vascular smooth muscle cells. Vascular smooth muscle cells from rat thoracic aorta were cultured by explant method. Subjects in this experiment were divided into eight groups: normal control group (group C), U-II group (group M), positive control group (Flu group) and urantide-treated groups (10⁻¹⁰, 10⁻⁹, 10⁻⁸, 10⁻⁷ and 10⁻⁶ mol/L). Cultured vascular smooth muscle cells in vitro were studied by immunocytochemistry, biochemistry, and flow cytometry. U-II (10⁻⁸ mol/L) promoted the proliferation of vascular smooth muscle cells at each time point, influenced cell cycle, increased proliferation index and S-phase cell fraction, and dramatically promoted the expression of U-II and GPR14. In the concentration range from 10⁻¹⁰ to 10⁻⁶ mol/L, urantide dramatically inhibited the proliferation of vascular smooth muscle cells and the protein expression of U-II and GPR14, especially at a concentration of 10⁻⁶ mol/L. U-II, binding with its receptor GPR14, promotes vascular smooth muscle cells proliferation and migration, which can be inhibited by urantide. This study provides an evidence for understanding the effects of U-II and its receptor GPR14 on vascular smooth muscle cells.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4333937PMC
http://dx.doi.org/10.17305/bjbms.2013.2369DOI Listing
May 2013

The role of the Rho/Rock signaling pathway in the pathogenesis of acute ischemic myocardial fibrosis in rat models.

Exp Ther Med 2013 Apr 30;5(4):1123-1128. Epub 2013 Jan 30.

Department of Clinical Pharmacy and Pharmaceutical Management, Jilin University, Changchun 130021;

The aim of this study was to investigate the role of the Rho/Rho associated coiled coil-forming protein kinase (Rock) signaling pathway in the pathogenesis of ischemic myocardial fibrosis (MF) in rats. The MF rat model was established using isoprenaline hydrochloride (ISO, 15 mg/kg). Rats were randomly divided into ten groups: a control group and ISO-treated groups at 2 h, 4 h, 6 h, 12 h, 24 h, 48 h, 72 h, 7 days and 21 days. The MF model was evaluated by serum enzyme levels, hematoxylin and eosin (H&E) staining and Masson's staining, . The mRNA expression of RhoA and Rock I was assessed with reverse transcription-polymerase chain reaction (RT-PCR). The cell type was evaluated by immunofluorescent and immunohistochemical staining. The protein expression of Rock I was evaluated using western blotting and immunohistochemistry. MF was found to be more developed in the ISO-treated group compared with the control group. CD31 and vimentin expression in fibroblasts and endothelial cells were significantly increased. In addition, the mRNA and protein levels of RhoA and Rock I were significantly increased. In conclusion, activation of Rho/Rock accelerates the degree of ischemic MF. Inhibition of Rho/Rock may be a novel therapeutic strategy for the prevention of ischemic MF.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3892/etm.2013.935DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3627446PMC
April 2013

Erythropoietin attenuates cardiac dysfunction by increasing myocardial angiogenesis and inhibiting interstitial fibrosis in diabetic rats.

Cardiovasc Diabetol 2012 Sep 7;11:105. Epub 2012 Sep 7.

Department and Institute of Cardiology, Zhongda Hospital, Medical School of Southeast University, 87 Dingjiaqiao street, Nanjing 210009, China.

Background: Recent studies revealed that erythropoietin (EPO) has tissue-protective effects in the heart by increasing vascular endothelial growth factor (VEGF) expression and attenuating myocardial fibrosis in ischemia models. In this study, we investigated the effect of EPO on ventricular remodeling and blood vessel growth in diabetic rats.

Methods: Male SD rats were randomly divided into 3 groups: control rats, streptozotocin (STZ)-induced diabetic rats, and diabetic rats treated with 1000 U/kg EPO by subcutaneous injection once per week. Twelve weeks later, echocardiography was conducted, and blood samples were collected for counting of peripheral blood endothelial progenitor cells (EPCs). Myocardial tissues were collected, quantitative real-time PCR (RT-PCR) was used to detect the mRNA expression of VEGF and EPO-receptor (EPOR), and Western blotting was used to detect the protein expression of VEGF and EPOR. VEGF, EPOR, transforming growth factor beta (TGF-β), and CD31 levels in the myocardium were determined by immunohistochemistry. To detect cardiac hypertrophy, immunohistochemistry of collagen type I, collagen type III, and Picrosirius Red staining were performed, and cardiomyocyte cross-sectional area was measured.

Results: After 12 weeks STZ injection, blood glucose increased significantly and remained consistently elevated. EPO treatment significantly improved cardiac contractility and reduced diastolic dysfunction. Rats receiving the EPO injection showed a significant increase in circulating EPCs (27.85 ± 3.43%, P < 0.01) compared with diabetic untreated animals. EPO injection significantly increased capillary density as well as EPOR and VEGF expression in left ventricular myocardial tissue from diabetic rats. Moreover, EPO inhibited interstitial collagen deposition and reduced TGF-β expression.

Conclusions: Treatment with EPO protects cardiac tissue in diabetic animals by increasing VEGF and EPOR expression levels, leading to improved revascularization and the inhibition of cardiac fibrosis.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1186/1475-2840-11-105DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3527329PMC
September 2012

Effect of fluoride on insulin level of rats and insulin receptor expression in the MC3T3-E1 cells.

Biol Trace Elem Res 2012 Dec 8;150(1-3):297-305. Epub 2012 Aug 8.

Department of Obstetrics and Gynecology, General Hospital of Bejing Military Region, Beijing, 100700, China.

Studies on the role of insulin and insulin receptor (InsR) in the process of skeletal fluorosis, especially in osteogenic function, are rare. We evaluated the effect of increasing F⁻ doses on the marker of bone formation, serum insulin level and pancreatic secretion changes in vivo and mRNA expression of InsR and osteocalcin (OCN) in vitro. Wistar rats (n = 50) were divided into two groups, i.e. a control group and fluoride group. The fluoride groups were treated with fluoride by drinking tap water containing 100 mg F⁻/L. The fluoride ion-selective electrode measured the fluoride concentrations of femurs. The alkaline phosphatase (ALP), OCN, insulin and glucagon of serum were tested to observe the effect of fluoride action on them. Meantime, the pancreas pathological morphometry analysis via β cells stained by aldehyde fuchsin showed the action of fluoride on pancreas secretion. MC3T3-E1 cells (derived from newborn mouse calvaria) were exposed to varying concentrations and periods of fluoride. The mRNA expression of InsR and OCN was quantified with real-time PCR. Results showed that 1-year fluoride treatment obviously stimulated ALP activity and OCN level along with increase of bone fluoride concentration of rats, which indicated that fluoride obviously stimulated osteogenic action of rats. In vitro study, the dual effect of fluoride on osteoblast function is shown. On the other hand, there was a significant increase of serum insulin level and a general decrease of glucagon level, and the histomorphometry analysis indicated an elevated insulin-positive area and increase in islet size in rats treated with fluoride for 1 year. In addition, fluoride obviously facilitated the mRNA expression of InsR in vitro. To sum up, there existed a close relationship between insulin secretion and fluoride treatment. The insulin signal pathway might be involved in the underlying occurrence or development of skeletal fluorosis.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1007/s12011-012-9482-xDOI Listing
December 2012

XPA A23G polymorphism and lung cancer risk: a meta-analysis.

Mol Biol Rep 2012 Feb 25;39(2):1435-40. Epub 2011 May 25.

Department of Gerontology, The Affiliated Zhong Da Hospital of Southeast University, 87 Dingjiaqiao, Nanjing 210009, People's Republic of China.

Case-control studies on the association between XPA A23G and lung cancer have provided either controversial or inconclusive results. To clarify the effect of XPA A23G on the risk of lung cancer, a meta-analysis of all case-control observational studies was performed. Pooled odds ratios (ORs) for various polymorphisms were estimated using random and fixed effects models. The Q-statistic was used to evaluate the homogeneity, and Egger and Begg tests were used to assess publication bias. For the homozygote GG and G allele carriers (GA + GG), the pooled ORs were 1.24 (95% CI 1.05-1.46; P = 0.27 for heterogeneity) and 1.30 (95% CI 1.13-1.51; P = 0.45 for heterogeneity) compared to the homozygous genotype (AA). In the stratified analysis by ethnicity, the ORs of the G allele carriers and the homozygote GG were 1.28 (95% CI 1.10-1.49; P = 0.07 for heterogeneity) and 1.42 (95% CI 1.04-1.93; P = 0.39 for heterogeneity) among non-Caucasians. No significant associations were found in the Caucasian population in any of the genetic models. When studies that were not in Hardy-Weinberg equilibrium (HWE) were corrected, the pattern of the results remained the same. Our results indicated a significantly decreased risk of lung cancer in non-Caucasians with the G allele.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1007/s11033-011-0878-zDOI Listing
February 2012

2D-DIGE proteomic analysis of changes in estrogen/progesterone-induced rat breast hyperplasia upon treatment with the Mongolian remedy RuXian-I.

Molecules 2011 Apr 8;16(4):3048-65. Epub 2011 Apr 8.

Department of Experimental Pharmacology and Toxicology, School of Pharmaceutical Sciences, Jilin University, Changchun 130021, China.

RuXian-I has traditionally been used as a remedy for breast hyperplasia in the Inner Mongolia Autonomous Region of China. As a first step toward the investigation of biomarkers associated with RuXian-I treatment, a proteome-wide analysis of rat breast tissue was conducted. First, rat breast hyperplasia was induced by injection of estradiol and progesterone. After treatment with RuXian-I, there is a marked decrease in the hyperplasia, as can be shown by decreases in the nipple diameter and the pathological changes in breast. Subsequently, we used an approach that integrates size-based 2D-DIGE, MALDI-TOF/TOF-MS, and bioinformatics to analyze data from the control group, the model group and the RuXian-I treatment group. Using this approach, seventeen affected proteins were identified. Among these, 15 (including annexin A1, annexin A2, superoxide dismutase [Mn], peroxiredoxin-1, translationally-controlled tumor protein and a B-crystallin) were significantly up-regulated in the model group and down-regulated upon treatment with RuXian-I, and two (Tpil protein and myosin-4) have the opposite change trend. The expression of annexin A1 was confirmed using immunohistochemistry. The expression of superoxide dismutase (SOD) activity was confirmed biochemically. These results indicated that RuXian-I treats rat breast hyperplasia through regulation of cell cycle, immune system, metabolic, signal transduction, etc. The differential expressions of these proteins (annexin A1, superoxide dismutase [Mn], alpha B-crystallins and translationally controlled tumor protein, among others) were associated with occurrence and metastasis of breast cancer. These findings might provide not only far-reaching valuable insights into the mechanism of RuXian-I action, but also leads for prognosis and diagnosis of breast hyperplasia and breast cancer.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3390/molecules16043048DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6260641PMC
April 2011

[Expression and implication of angiotensin II type 1 receptor in myocardial fibrosis of rats].

Zhonghua Bing Li Xue Za Zhi 2008 Oct;37(10):687-92

Department of Pathology, School of Pharmacy, Jilin University, Changchun 130021, China.

Objective: To investigate the expression and pathobiological implications of angiotensin II type 1 receptor (AT1R) in development of myocardial fibrosis of rats.

Methods: Rat myocardial necrosis model was established using isoproterenol injection (15 mg/kg). Rat serum aspartate transaminase (AST), lactate dehydrogenase (LDH), creatine kinase (CK) and creatine kinase isoenzymes (CK-MB) were detected by MD-100 automatic biochemical analyzer. Masson staining was used to evaluate the morphological changes. The expression of AT1R protein was determined by immunohistochemistry and its mRNA expression was analyzed by RT-PCR. The expression of collage type I and III was determined by immunohistochemistry.

Results: Serum LDH, CK and CK-MB reached their peaks at 4 h (chi2 = 16.90, P < 0.05), and AST achieved its peak in 6 h (chi2 = 16.90, P < 0.05). AT1R mRNA expression was increased 2 - 12 h after isoproterenol injection, but no statistical significance (P > 0.05) was observed comparing with the control. However, a significant AT1R mRNA increase was present at 24 h and decreased gradually after 48 h, and back to the control level after 3 weeks. Protein expression of AT1R increased proportionally with the severity of the fibrosis.

Conclusions: AT1R mRNA and protein expressions increase significantly during myocardial ischemia, and is closely correlated with the fibrosis. These findings indicate that AT1R may play an important role in the pathogenesis of myocardial fibrosis.
View Article and Find Full Text PDF

Download full-text PDF

Source
October 2008

[Application of flow cytometric immunophenotypic analysis in the diagnosis of malignant lymphoma].

Zhonghua Xue Ye Xue Za Zhi 2007 Oct;28(10):671-6

Department of Pathology, Cancer Hospital/Institute, CAMS & PUMC, Beijing 100021, China.

Objective: To explore the value of flow cytometric immunophenotyping (FCI) in the diagnosis and differentiated diagnosis of lymphoma and explain the immunophenotypic features and differences of malignant lymphoma.

Methods: Seventy four fresh samples of suspicious lymphoma were collected from Nov. 2004 to Aug. 2006. Each sample was individually evaluated by FCI. The results were analyzed and compared with the histopathological diagnosis.

Results: Among the 74 cases, the FCI data consisted with the final morphological diagnosis in 61 cases (82.4%). For the diagnosis of B and T non-Hodgkin's lymphoma (NHL), thymoma, carcinoma and benign lesions of lymph node, the concordance between FCI data and morphological diagnosis were 93.5%, 100%, 100%, 100% and 81.3%, respectively.

Conclusion: Multi-parameter FCI analysis can provide important information and help for diagnosis of lymphoma. It is an assistant but necessary approach for the diagnosis and differential diagnosis of lymphoma.
View Article and Find Full Text PDF

Download full-text PDF

Source
October 2007

[Expression of annexin I in different histological types of carcinomas].

Zhonghua Zhong Liu Za Zhi 2007 Jun;29(6):444-8

Department of Pathology, Cancer Hospital (Institute), Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100021, China.

Objective: To investigate the expression of annexin I in esophageal squamous cell carcinoma (SCC) and carcinomas of other histological types in order to analyze the correlation between the expression of annexin I and carcinogenesis.

Methods: First, a set of tissue microarray was established, which consisted of SCC from the esophagus (208 cases), lung, larynx, cervix, and external genital organs; adenocarcinomas from the lung, stomach, colon and rectum, liver, pancreas, breast, thyroid and kidney with 30 cases in each group, meanwhile, the corresponding normal tissue was also obtained for control. Immunohistochemistry was used to detect the expression of annexin I in different types of carcinomas and the corresponding normal controls from different organs. The correlation between the expression of annexin I and the clinicopathological feature was analyzed and compared, which included age, gender, differentiation grade and lymph node metastasis.

Results: It was found that the expression of annexin I was decreased in esophageal SCC, when compared with normal esophageal squamous epithelia (P < 0.001), the similarity was also found in SCC of the lung, larynx and cervix. However, though negative in normal epidermis, annexin I expression was detected in some cases with SCC from external genital organs. Annexin I was found to be overexpressed in adenocarcinomas of the lung, stomach, colon and rectum, liver, pancreas, breast, thyroid and kidney, particularly very strong expression of annexin I was seen in lung adenocarcinoma, uterine endometrioid adenocarcinoma and ovarian serous adenocarcinoma. Interestingly, it was found to be positive in all thyroid papillary carcinomas, but negative in all normal thyroid glands. However, annexin I expression was found to be negative in all hepatocellular carcinoma and normal hepatocytes; and it was only detected in myoepithelium of normal breast tissue, but not in ductal luminal cells, and rarely in infiltrating ductal adenocarcinoma. In SCC, annexin I expression was stronger in well differentiated ones than that in the poorly differentiated ones. However, contrasting with SCC, in the adenocarcinomas from different organs, annexin I expression was much stronger in poorly differentiated ones than that in the well differentiate ones, especially in the adenocarcinomas from stomach, colon and rectum, pancreas, ovarian and kidney.

Conclusion: Annexin I expression is quite different among different types of carcinomas, and is correlated with histopathological type and differentiation grade. Further study is needed to investigate its role in the carcinogenesis.
View Article and Find Full Text PDF

Download full-text PDF

Source
June 2007

[Influence of recombined human growth hormone on sIgA and EGF in rats with obstructive jaundice].

Zhongguo Ying Yong Sheng Li Xue Za Zhi 2007 May;23(2):241-4

1st Affiliated Hospital, University of Henan Science and Technology, Henan 471003, China.

Aim: To study the effect of the recombined human growth hormone(rhGH) on secretory immunoglobulin A (sIgA), epidermal growth factor (EGF) in rats with obstructive jaundice.

Methods: Sixty Wistar rats were randomly divided into four groups, sham-operated (group A), common biliary duct-ligated (group B), biliary duct-ligated plus rhGH-treat for one week (group C), biliary duct-ligated plus rhGH-treat for two weeks (group D), each group had 15 rats. Except group A, the rats of other groups were operated with biliary duct-ligated. Until two weeks after operation, the rats of group A and B were killed. After operation, the rats of group C were treated with rhGH hypodermic injection (0.75 U x kg(-1) x d(-1)) for one week, and then killed. The rats of D group were treated with rhGH hypodermic injection (0.75 U x kg(-1) x d(-1)) for two weeks, and then killed. All procedures were performed aseptically. Total bilirubin (TB), alkaline phosphatase (ALP), prealbumin(PA), insulin-like growth factor (IGF-1), sIgA, EGF were measured.

Results: Compared with group A, in group B, C, D, serum level of PA, IGF-1 and sIgA, EGF level of gastric and intestinal juice were lower, but TB, ALP were higher, there were significant difference. Compared with group B, the rats with treatment of rhGH in group C and D had higher sIgA and EGF and lower intestinal bacterial translocation.

Conclusion: In objective jaundice rats, rhGH can protect their hepatic function, intestinal physical-barrier function and immune-barrier function, and reduce intestinal bacterial translocation.
View Article and Find Full Text PDF

Download full-text PDF

Source
May 2007

[Expression of Fas, Fas ligand, Fas-associated death domain protein, caspase 8 and mutant P53 protein in esophageal squamous cell carcinoma].

Zhonghua Yi Xue Za Zhi 2007 Jan;87(3):150-4

Department of Pathology, Cancer Institute (Hospital), Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing 100021, China.

Objective: To investigate the expression of five apoptosis-related proteins, Fas, Fas ligand (FasL), Fas-associated death domain protein (FADD), caspase 8, and mutant p53, in human esophageal squamous cell carcinoma (ESCC) tissue, and analyze the association of these proteins with ESCC malignant progression.

Methods: 116 ESCC specimens obtained during operation. Tissue microarray composed of the 116 specimens of cancerous tissues and corresponding paracancerous normal epithelium tissues was constructed. The expression of Fas, FasL, FADD, caspase 8, and mutant p53 was detected in the ESCC tissues and paracancerous normal epithelium tissues and analysis was conducted for the correlation between the expression of these proteins and the pathoclinical features and prognosis. involvement, differentiated grade, pTNM stages and disease-free survival.

Results: The positive rate of Fas in the ESCC tissues was 41.4%, significantly lower than that in the normal squamous epithelium was 95.7%, P < 0.001). The positive rates of FasL and FADD in the ESCC tissues were 76.7% and 50.0%, both significantly higher than those in the normal squamous epithelium (39.7% and 7.8%, both P < 0.001). Caspase 8 was strongly positive in the whole normal esophageal epithelium tissue except basal and superbasal cells, but negative in ESCC. Mutant p53 protein was negative in the normal esophageal epithelium tissue, with only several cases positive in the basal cells, but was diffusely positive in ESCC tissues with a positive rate of 37.1%. The expression of Fas in the well and moderately differentiated ESCC tissues was significantly higher than in the poorly differentiated ones (P = 0.022). The patients with positive expression of FADD had lower disease-free survival rate (P = 0.0028). The expression of Fas, FasL, caspase 8, and mutant p53 was not related with disease-free survival rate (P > 0.05).

Conclusion: The apoptosis-related markers, such as Fas, FasL, FADD, caspase 8, and mutant p53 protein may play important roles in the development and progression of ESCC, and FADD can be used as a marker to predict the advance and prognosis of ESCC.
View Article and Find Full Text PDF

Download full-text PDF

Source
January 2007

Clinical features of renal artery stenosis in elderly patients.

Chin Med J (Engl) 2007 Feb;120(4):345-7

Institute of Nephrology, Zhong Da Hospital, Southeast University, Nanjing 210009, China.

View Article and Find Full Text PDF

Download full-text PDF

Source
February 2007

Tissue microarray analysis reveals a tight correlation between protein expression pattern and progression of esophageal squamous cell carcinoma.

BMC Cancer 2006 Dec 22;6:296. Epub 2006 Dec 22.

Department of Pathology, Cancer Institute (Hospital), Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, China.

Background: The development of esophageal squamous cell carcinoma (ESCC) progresses a multistage process, collectively known as precursor lesions, also called dysplasia (DYS) and carcinoma in situ (CIS), subsequent invasive lesions and final metastasis. In this study, we are interested in investigating the expression of a variety of functional classes of proteins in ESCC and its precursor lesions and characterizing the correlation of these proteins with ESCC malignant progression.

Methods: Fas, FADD, caspase 8, CDC25B, fascin, CK14, CK4, annexin I, laminin-5gamma2 and SPARC were analyzed using immunohistochemistry on tissue microarray containing 205 ESCC and 173 adjacent precursor lesions as well as corresponding normal mucosa. To confirm the immunohistochemical results, three proteins, fascin, CK14 and laminin-5gamma2, which were overexpressed in ESCC on tissue microarray, were detected in 12 ESCC cell lines by Western blot assay.

Results: In ESCC and its precursor lesions, FADD, CDC25B, fascin, CK14, laminin-5gamma2 and SPARC were overexpressed, while Fas, caspase 8, CK4 and annexin I were underexpressed. The abnormalities of these proteins could be classified into different groups in relation to the stages of ESCC development. They were "early" corresponding to mild and moderate DYS with overexpression of fascin, FADD and CDC25B and underexpression of Fas, caspase 8, CK4 and annexin I, "intermediate" to severe DYS and CIS with overexpression of FADD and CK14, and "late" to invasive lesions (ESCC) and to advanced pTNM stage ESCC lesions with overexpression of CK14, laminin-5gamma2 and SPARC.

Conclusion: Analyzing the protein expression patterns of Fas, FADD, caspase 8, CDC25B, fascin, CK14, CK4, annexin I, laminin-5gamma2 and SPARC would be valuable to develop rational strategies for early detection of lesions at risk in advance as well as for prevention and treatment of ESCC.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1186/1471-2407-6-296DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1766359PMC
December 2006

[Glomus tumor of the trachea].

Authors:
Li-Qun Ren Ning Lü

Zhonghua Bing Li Xue Za Zhi 2005 Feb;34(2):124-5

View Article and Find Full Text PDF

Download full-text PDF

Source
February 2005