Publications by authors named "Yijun Zeng"

31 Publications

A Review of Foreign Language Enjoyment and Engagement.

Authors:
Yijun Zeng

Front Psychol 2021 12;12:737613. Epub 2021 Aug 12.

Department of International Business, Hainan College of Foreign Studies, Wenchang, China.

The introduction of positive psychology into foreign/second language learning has led to a multitude of novel theoretical and empirical studies. Foreign language enjoyment (FLE) is regarded as a response to the widely examined concept of classroom anxiety. The majority of these studies have investigated the effect of learners' and teachers' characteristics (Xie and Derakhshan, 2021) pertaining to FLE on learners' academic achievement and their engagement in classroom tasks. Following a seminal study by Dewaele and MacIntyre (2014) and the development of the primary FLE scale, some researchers evaluated the extent of learners' enjoyment in the language learning environment; these studies approved the effectiveness and prominence of FLE throughout the learning process. The present review is an attempt to review studies on FLE during the past two decades. The related literature confirms the significance and efficiency of promoting FLE in the classroom because it brings about higher levels of motivation and engagement among language learners and leads to prolonged success and achievement. A summary of the major efforts regarding this area of research is presented in this study.
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http://dx.doi.org/10.3389/fpsyg.2021.737613DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8397506PMC
August 2021

Culprit vascular patterns and surgical outcomes of hemifacial spasm caused by an AICA segment passing between cranial nerve VII and VIII: A series of 25 cases.

Clin Neurol Neurosurg 2021 08 24;207:106777. Epub 2021 Jun 24.

Department of Neurosurgery, West China Hospital of Sichuan University, Chengdu, China. Electronic address:

Objective: To report the vascular anatomic characteristics and surgical outcomes of hemifacial spasm (HFS) caused by an anterior inferior cerebellar artery (AICA) segment passing between cranial nerve VII (CN VII) and cranial nerve VIII (CN VIII).

Patients And Methods: This case series study retrospectively reviewed records of 1040 consecutive patients treated with MVD for HFS in our hospital in 10 years. 25 patients had the culprit vessel recorded as an AICA segment passing between CN VII and CN VIII. Vascular anatomic characteristics were reviewed from intraoperative microscopic videos. The clinical outcomes were followed up at 3-month and 1-year time points.

Results: The culprit AICA segments feature 3 discrete anatomic patterns. The patterns denoted as pattern A, B, and C were identified in 19(76%), 3(12%), and 3 (12%) of the 25 patients respectively. Postoperative spasm relief were achieved in 19(76%), 22(88%), and 23 (92%) of the patients at immediately after surgery, 3-month, and 1-year follow-up respectively. 3(12%) of them have permanent postoperative cranial nerve deficits, including one patient with hearing loss and 2 patients with vocal cord palsy.

Conclusions: Though an AICA segment passing between CN VII and CN VIII is common, very rarely it was deemed the culprit for HFS in our patients. We used fREZ centered definition and operation. We found the culprit AICA segments feature 3 discrete anatomic patterns. We observed good spasm relief outcome and relatively fewer complications with CN VII and CN VIII. Identifying the 3 anatomic patterns may help with a smooth decision-making when vascular compression by an AICA segment passing between CN VII and CN VIII is suspected.
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http://dx.doi.org/10.1016/j.clineuro.2021.106777DOI Listing
August 2021

Urine miR-93-5p is a promising biomarker for early detection of HBV-related hepatocellular carcinoma.

Eur J Surg Oncol 2021 Jun 13. Epub 2021 Jun 13.

Department of Emergency Medicine, The First Affiliated Hospital of Gannan Medical University, Ganzhou, 341000, China. Electronic address:

Introduction: The mortality rate of hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC)continues to increase because sensitive, early and readily available diagnostic tools are lacking. To address this problem, we aimed to identify diagnosticbio markers to be used for early detection of HCC.

Materials And Methods: miR-93-5p was selected as a candidate biomarker based on the analyses of relevant Gene Expression Omnibus (GEO) datasets; it was validated using qPCR to quantify its expression levels in tissue, plasma and saliva sample sets.

Results: miR-93-5p was significantly upregulated in HBV-related HCC tissue. Notably, miR-93-5p in plasma and urine was also significantly increased in patients with early HBV-related HCC. The expression of miR-93-5p was significantly and positively correlated in pairwise comparisons of samples (tissue vs. plasma, tissue vs. urine, plasma vs. urine). Moreover, after curative hepatectomy,miR-93-5p in plasma and urine decreased significantly over one month after the curative hepatectomy and returned to normal levels. Furthermore, receiver operating characteristic (ROC) analysis indicated that both plasma and urine miR-39-5p could detect be used to early, advanced and overall HBV-related HCC cases with more than 85% sensitivities and 93% of specificities. Finally, urine miR-93-5p could be used to predict progress-free survival for early HCC patients who received curative hepatectomy and overall survival for advanced HCC patients without curative treatments.

Conclusions: Plasma and urine miR-93-5p show great promise as potential novel biomarkers for early detection of HBV-related HCC. Moreover, urine miR-93-5p could be used to predict the prognosis of patients with HBV-related HCC.
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http://dx.doi.org/10.1016/j.ejso.2021.06.015DOI Listing
June 2021

Drug delivery systems for elemene, its main active ingredient β-elemene, and its derivatives in cancer therapy.

Int J Nanomedicine 2018 10;13:6279-6296. Epub 2018 Oct 10.

Holistic Integrative Pharmacy Institutes, Hangzhou Normal University, Hangzhou, Zhejiang, China,

β-elemene is a noncytotoxic Class II antitumor drug extracted from the traditional Chinese medicine Y. H. Chen et C. Ling. β-elemene exerts its effects by inhibiting cell proliferation, arresting the cell cycle, inducing cell apoptosis, exerting antiangiogenesis and antimetastasis effects, reversing multiple-drug resistance (MDR), and enhancing the immune system. Elemene injection and oral emulsion have been used to treat various tumors, including cancer of the lung, liver, brain, breast, ovary, gastric, prostate, and other tissues, for >20 years. The safety of both elemene injection and oral emulsion in the clinic has been discussed. Recently, the secondary development of β-elemene has attracted the attention of researchers and made great progress. On the one hand, studies have been carried out on liposome-based systems (including solid lipid nanoparticles [SLNs], nanostructured lipid carriers [NLCs], long-circulating liposomes, active targeting liposomes, and multidrug-loaded liposomes) and emulsion systems (including microemulsions, self-emulsion drug delivery systems [SEDDSs], and active targeting microemulsion) to solve the issues of poor solubility in water, low bioavailability, and severe phlebitis, as well as to improve antitumor efficacy. The pharmacokinetics of different drug delivery systems of β-elemene are also summarized. On the other hand, a number of highly active anticancer β-elemene derivatives have been obtained through modification of the structure of β-elemene. This review focuses on the two drug delivery systems and derivatives of β-elemene for cancer therapy.
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http://dx.doi.org/10.2147/IJN.S174527DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6186893PMC
December 2018

The PPARγ agonist rosiglitazone sensitizes the BH3 mimetic (-)-gossypol to induce apoptosis in cancer cells with high level of Bcl-2.

Mol Carcinog 2018 09 12;57(9):1213-1222. Epub 2018 Jun 12.

Department of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Army Medical University (Third Military Medical University), Chongqing, China.

The BH3 mimetic (-)-gossypol (-)-G has shown promising efficacy to kill several kinds of cancer cells or potentiate current chemotherapeutics. But it induces limited apoptosis in cancer cells with high level of Bcl-2. The nuclear receptor PPARγ and its agonist rosiglitazone can suppress various malignancies. More importantly, rosiglitazone is able to enhance the anti-tumor effects of chemotherapy drugs such as carboplatin and tyrosine kinase inhibitors. In this study, we for the first time demonstrated that rosiglitazone could sensitize (-)-G to induce apoptosis in cancer cells with high level of Bcl-2. Furthermore, we found that (-)-G increased the mRNA level and protein stability of Mcl-1, which weakened the pro-apoptotic effect of (-)-G. Rosiglitazone attenuated the (-)-G-induced Mcl-1 stability through decreasing JNK phosphorylation. Additionally, rosiglitazone upregulated dual-specificity phosphatase 16 (DUSP16), leading to a reduction of (-)-G-triggered JNK phosphorylation. Animal experiments showed that rosiglitazone could sensitize (-)-G to repress the growth of cancer cells with high level of Bcl-2 in vivo. Taken together, our results suggest that the PPARγ agonists may enhance the therapeutic effect of BH3 mimetics in cancers with high level of Bcl-2 through regulating the DUSP16/JNK/Mcl-1 singling pathway. This study may provide novel insights into the cancer therapeutics based on the combination of PPARγ agonists and BH3 mimetics.
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http://dx.doi.org/10.1002/mc.22837DOI Listing
September 2018

Induction of SOCS3 by liver X receptor suppresses the proliferation of hepatocellular carcinoma cells.

Oncotarget 2017 Sep 18;8(38):64083-64094. Epub 2017 Jul 18.

Department of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Third Military Medical University, Chongqing 400038, China.

Liver X receptor (LXR), a member of nuclear receptor superfamily, is involved in the regulation of glucose, lipid and cholesterol metabolism. Recently, it has been reported that LXR suppress different kinds of cancers including hepatocellular carcinoma (HCC). However, the corresponding mechanism is still not well elucidated. In the present study, we found that activation of LXR downregulated cyclin D1 while upregulated p21 and p27 by elevating the level of suppressor of cytokine signaling 3 (SOCS3), leading to the cell cycle arrest at G1/S phase and growth inhibition of HCC cells. Moreover, we demonstrated that LXRα (not LXRβ) mediated the induction of SOCS3 in HCC cells. Subsequently, we showed that LXR activation enhanced the mRNA stability of SOCS3, but had no significant influence on the transcriptional activity of gene promoter. The experiments in nude mice revealed that LXR agonist inhibited the growth of xenograft tumors and enhanced SOCS3 expression . These results indicate that "LXRα-SOCS3-cyclin D1/p21/p27" is a novel pathway by which LXR exerts its anti-HCC effects, suggesting that the pathway may be a new potential therapeutic target for HCC treatment.
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http://dx.doi.org/10.18632/oncotarget.19321DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5609985PMC
September 2017

HSF1 upregulates ATG4B expression and enhances epirubicin-induced protective autophagy in hepatocellular carcinoma cells.

Cancer Lett 2017 11 6;409:81-90. Epub 2017 Sep 6.

Department of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Third Military Medical University, Chongqing 400038, China. Electronic address:

Considerable evidences have shown that both heat shock transcription factor 1 (HSF1) and autophagy can attenuate the sensitivity of hepatocellular carcinoma (HCC) cells to chemotherapeutic reagents. However, it is still little known whether HSF1 is associated with autophagy in regulating the chemosensitivity of HCC cells. In this study, we for the first time demonstrated that HSF1 markedly attenuated the killing effect of epirubicin (EPI) to HCC cells via enhancing the EPI-induced protective autophagy. Mechanistically, HSF1 upregulated autophagy related 4B (ATG4B) in HCC cells, which enhanced the EPI-triggered protective autophagy. Reporter assay showed that HSF1 increased the transcriptional activity of ATG4B gene promoter, and chromatin immunoprecipitation assay verified that HSF1 bound to the site (-1429 to -1417) in ATG4B gene promoter region. The experiments in nude mice showed that knockdown of HSF1 or ATG4B strengthened the anti-HCC effect of EPI in vivo. Collectively, these results revealed that HSF1 elevates ATG4B via promoting its transcription, which alleviates the sensitivity of EPI in HCC cells through enhancing protective autophagy, suggesting that the "HSF1/ATG4B/protective autophagy" pathway may be a novel target for developing sensitizing strategy to HCC chemotherapy.
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http://dx.doi.org/10.1016/j.canlet.2017.08.039DOI Listing
November 2017

Inhibition of COX2 enhances the chemosensitivity of dichloroacetate in cervical cancer cells.

Oncotarget 2017 Aug 16;8(31):51748-51757. Epub 2017 Jun 16.

Department of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Third Military Medical University, Chongqing 400038, China.

Dichloroacetate (DCA), a traditional mitochondria-targeting agent, has shown promising prospect as a sensitizer in fighting against malignancies including cervical cancer. But it is unclear about the effect of DCA alone on cervical tumor. Moreover, previous reports have demonstrated that the increased cyclooxygenase-2 (COX2) expression is associated with chemoresistance and poor prognosis of cervical cancer. However, it is still unknown whether COX2 can affect the sensitivity of DCA in cervical cancer cells. In this study, we found that cervical cancer cells were insensitive to DCA. Furthermore, we for the first time revealed that DCA could upregulate COX2 which impeded the chemosensitivity of DCA in cervical cancer cells. Mechanistic study showed that DCA reduced the level of RNA binding protein quaking (QKI), leading to the decay suppression of COX2 mRNA and the subsequent elevation of COX2 protein. Inhibition of COX2 using celecoxib could sensitize DCA in repressing the growth of cervical cancer cells both and . These results indicate that COX2 is a novel resistance factor of DCA, and combination of celecoxib with DCA may be beneficial to the treatment of cervical cancer.
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http://dx.doi.org/10.18632/oncotarget.18518DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5584284PMC
August 2017

lncRNA HULC promotes the growth of hepatocellular carcinoma cells via stabilizing COX-2 protein.

Biochem Biophys Res Commun 2017 08 17;490(3):693-699. Epub 2017 Jun 17.

Department of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Third Military Medical University, Chongqing 400038, China. Electronic address:

Highly upregulated in liver cancer (HULC), a lncRNA overexpressed in hepatocellular carcinoma (HCC), has been demonstrated to be involved in the carcinogenesis and progression of HCC. However, the mechanisms of HULC promoting the abnormal growth of HCC cells are still not well elucidated. In the present study, we for the first time demonstrated that HULC promoted the growth of HCC cells through elevating COX-2 protein. Moreover, the study of the corresponding mechanism by which HULC upregulated COX-2 showed that HULC enhanced the level of ubiquitin-specific peptidase 22 (USP22), which decreased ubiquitin-mediated degradation of COX-2 protein by removing the conjugated polyubiquitin chains from COX-2 and finally stabilized COX2 protein. In addition, knockdown of USP22 or COX-2 attenuated HULC-mediated abnormal growth of HCC cells. In conclusion, our results demonstrated that "USP22/COX-2" axis played an important role in HULC promoting growth of HCC cells. The identification of this novel pathway may pave a road for developing new potential anti-HCC strategies.
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http://dx.doi.org/10.1016/j.bbrc.2017.06.103DOI Listing
August 2017

Metformin Synergizes with BCL-XL/BCL-2 Inhibitor ABT-263 to Induce Apoptosis Specifically in p53-Defective Cancer Cells.

Mol Cancer Ther 2017 09 22;16(9):1806-1818. Epub 2017 May 22.

Department of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Third Military Medical University, Chongqing, China.

p53 deficiency, a frequent event in multiple kinds of malignancies, decreases the sensitivity of diverse targeted chemotherapeutics including the BCL-XL/BCL-2 inhibitor ABT-263. Loss of p53 function can activate mTOR complex 1 (mTORC1), which may make it a vulnerable target. Metformin has shown anti-neoplastic efficiency partially through suppressing mTORC1. However, it remains unknown whether mTORC1 activation confers ABT-263 resistance and whether metformin can overcome it in the p53-defective contexts. In this study, we for the first time demonstrated that metformin and ABT-263 synergistically elicited remarkable apoptosis through orchestrating the proapoptotic machineries in various p53-defective cancer cells. Mechanistic studies revealed that metformin sensitized ABT-263 via attenuating mTORC1-mediated cap-dependent translation of and and weakening internal ribosome entry site (IRES)-dependent translation of Meanwhile, ABT-263 sensitized metformin through disrupting the BCL-XL/BIM complex. However, metformin and ABT-263 had no synergistic killing effect in p53 wild-type (p53-WT) cancer cells because the cotreatment dramatically induced the senescence-associated secretory phenotype (SASP) in the presence of wild type p53, and SASP could aberrantly activate the AKT/ERK-mTORC1-4EBP1-MCL-1/survivin signaling axis. Blocking the axis using corresponding kinase inhibitors or neutralizing antibodies against different SASP components sensitized the cotreatment effect of metformin and ABT-263 in p53-WT cancer cells. The experiments showed that metformin and ABT-263 synergistically inhibited the growth of p53-defective (but not p53-WT) cancer cells in tumor xenograft nude mice. These results suggest that the combination of metformin and ABT-263 may be a novel targeted therapeutic strategy for p53-defective cancers. .
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http://dx.doi.org/10.1158/1535-7163.MCT-16-0763DOI Listing
September 2017

Chicoric acid suppresses BAFF expression in B lymphocytes by inhibiting NF-κB activity.

Int Immunopharmacol 2017 Mar 22;44:211-215. Epub 2017 Jan 22.

Department of Biochemistry and Molecular Biology, College of Basic Medical Science, Third Military Medical University, Chongqing 400038, China. Electronic address:

B cell activating factor belonging to the TNF family (BAFF) plays a critical role in the pathogenesis of autoimmune diseases. The inhibition of BAFF expression is an emerging therapeutic approach for these disorders. Chicoric acid (CA), a bioactive phytochemical found in several widely used traditional medicinal plants, has significant anti-inflammatory activity and anti-arthritic effects. However, the role of CA in modulation of BAFF expression remains unknown. In this study, we demonstrated that CA reduced BAFF expression in human B lymphocyte cell lines and decreased the DNA-binding activity of nuclear factor-κB (NF-κB) in the BAFF promoter region. Furthermore, CA inhibited both the nuclear translocation of p65 (the subunit of NF-κB) and the phosphorylation of IκBα (inhibitor of NF-κB). These results suggest that CA suppresses BAFF expression by inhibiting NF-κB activity, and CA may serve as a novel therapeutic agent to down-regulate excessive BAFF expression in autoimmune diseases.
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http://dx.doi.org/10.1016/j.intimp.2017.01.021DOI Listing
March 2017

Dichloroacetate and metformin synergistically suppress the growth of ovarian cancer cells.

Oncotarget 2016 Sep;7(37):59458-59470

Department of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Third Military Medical University, Chongqing 400038, China.

Both dichloroacetate (DCA) and metformin (Met) have shown promising antitumor efficacy by regulating cancer cell metabolism. However, the DCA-mediated protective autophagy and Met-induced lactate accumulation limit their tumor-killing potential respectively. So overcoming the corresponding shortages will improve their therapeutic effects. In the present study, we found that DCA and Met synergistically inhibited the growth and enhanced the apoptosis of ovarian cancer cells. Interestingly, we for the first time revealed that Met sensitized DCA via dramatically attenuating DCA-induced Mcl-1 protein and protective autophagy, while DCA sensitized Met through markedly alleviating Met-induced excessive lactate accumulation and glucose consumption. The in vivo experiments in nude mice also showed that DCA and Met synergistically suppressed the growth of xenograft ovarian tumors. These results may pave a way for developing novel strategies for the treatment of ovarian cancer based on the combined use of DCA and Met.
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http://dx.doi.org/10.18632/oncotarget.10694DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5312324PMC
September 2016

Activation of LXR attenuates collagen-induced arthritis via suppressing BLyS production.

Clin Immunol 2015 Dec 1;161(2):339-47. Epub 2015 Oct 1.

Department of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Third Military Medical University, Chongqing 400038, China. Electronic address:

B-lymphocyte stimulator (BLyS) plays a critical role in the pathogenesis and progression of rheumatoid arthritis (RA). Liver X receptor (LXR), a nuclear receptor, has an important anti-inflammatory effect. However, it is unclear whether the BLyS expression is regulated by LXR. In this study, we found that treatment with LXR agonist in collagen-induced arthritis (CIA) mice significantly attenuated arthritis progression, and markedly decreased BLyS production in serum and splenocytes as well as the production of serum IFNγ and TGFβ. Activation of LXR in B lymphocytes dramatically suppressed the basal and IFNγ/TGFβ-induced BLyS expression. Moreover, LXR agonist prominently suppressed the binding of NF-κB to BLyS promoter region, and decreased the promoter's transcriptional activity. Additionally, activation of LXR obviously repressed IFNγ-induced STAT1 activation and TGFβ-induced SMAD3 activation. These results indicated that downregulation of BLyS may be a novel mechanism by which LXR ameliorates RA, and LXR/BLyS pathway may serve as a novel target for the treatment of RA.
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http://dx.doi.org/10.1016/j.clim.2015.09.015DOI Listing
December 2015

FXR induces SOCS3 and suppresses hepatocellular carcinoma.

Oncotarget 2015 Oct;6(33):34606-16

Department of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Third Military Medical University, Chongqing 400038, China.

Suppressor of cytokine signaling 3 (SOCS3) is regarded as a vital repressor in the liver carcinogenesis mainly by inhibiting signal transducer and activator of transcription 3 (STAT3) activity. Farnesoid X Receptor (FXR), highly expressed in liver, has an important role in protecting against hepatocellular carcinoma (HCC). However, it is unclear whether the tumor suppressive activity of FXR involves the regulation of SOCS3. In the present study, we found that activation of FXR by its specific agonist GW4064 in HCC cells inhibited cell growth, induced cell cycle arrest at G1 phase, elevated p21 expression and repressed STAT3 activity. The above anti-tumor effects of FXR were dramatically alleviated by knockdown of SOCS3 with siRNA. Reporter assay revealed that FXR activation enhanced the transcriptional activity of SOCS3 promoter. Electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation (ChIP) assay displayed that FXR directly bound to IR9 DNA motif within SOCS3 promoter region. The in vivo study in nude mice showed that treatment with FXR ligand GW4064 could decelerate the growth of HCC xenografts, up-regulate SOCS3 and p21 expression and inhibit STAT3 phosphorylation in the xenografts. These results suggest that induction of SOCS3 may be a novel mechanism by which FXR exerts its anti-HCC effects, and the FXR-SOCS3 signaling may serve as a new potential target for the prevention/treatment of HCC.
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http://dx.doi.org/10.18632/oncotarget.5314DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4741476PMC
October 2015

Upregulation of microRNA-122 by farnesoid X receptor suppresses the growth of hepatocellular carcinoma cells.

Mol Cancer 2015 Aug 25;14:163. Epub 2015 Aug 25.

Department of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Third Military Medical University, Chongqing, 400038, China.

Background: microRNA-122 (miR-122) is the most abundant and specific miRNA in the liver. It acts as an important tumor suppressor in hepatocellular carcinoma (HCC) through regulating its target genes, but details of its own regulation are largely unknown. Farnesoid X receptor (FXR), a transcription factor with multiple functions, plays an important role in protecting against liver carcinogenesis, but it is unclear whether the anti-HCC effect of FXR is involved in the regulation of miR-122.

Methods: The levels of miR-122 and FXR in HCC tissues and cell lines were examined by quantitative real-time PCR (qRT-PCR). qRT-PCR was also used to detect the expression of miR-122 target genes at mRNA level, while Western blotting was used to analyze that of their protein products. The effect of FXR on the transcriptional activity of miR-122 promoter was evaluated by a luciferase reporter assay. Electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation (ChIP) assay were performed to identify the FXR binding site within miR-122 promoter region. The cell proliferation was analyzed by a CCK-8 assay. The influence of FXR on tumor growth and miR-122 expression in vivo was monitored using HCC xenografts in nude mice.

Results: The expression of FXR was positively correlated with that of miR-122 in HCC tissues and cell lines. Activation of FXR in HCC cells upregulated miR-122 expression and in turn downregulated the expression of miR-122 target genes including insulin-like growth factor-1 receptor and cyclin G1. FXR bound directly to the DR2 element (-338 to -325) in miR-122 promoter region, and enhanced the promoter's transcriptional activity. Functional experiments showed that the FXR-mediated upregulation of miR-122 suppressed the proliferation of HCC cells in vitro and the growth of HCC xenografts in vivo.

Conclusions: miR-122 is a novel target gene of FXR, and the upregulation of miR-122 by FXR represses the growth of HCC cells, suggesting that FXR may serve as a key transcriptional regulator for manipulating miR-122 expression, and the FXR/miR-122 pathway may therefore be a novel target for the treatment of HCC.
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http://dx.doi.org/10.1186/s12943-015-0427-9DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4547435PMC
August 2015

MicroRNA-363-mediated downregulation of S1PR1 suppresses the proliferation of hepatocellular carcinoma cells.

Cell Signal 2014 Jun 12;26(6):1347-54. Epub 2014 Mar 12.

Department of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Third Military Medical University, Chongqing 400038, China. Electronic address:

S1PR1 plays a crucial role in promoting proliferation of hepatocellular carcinoma (HCC). Over expression of S1PR1 is observed in HCC cell lines. The mechanisms underlying the aberrant expression of S1PR1 are not known well. MircroRNAs are important regulators of gene expression and disproportionate microRNAs can result in dysregulation of oncogenes in cancer cells. In this study, we found that miR-363, a potential tumor suppressor microRNA, downregulated the expression of S1PR1 and inhibited the proliferation of HCC cells. Bioinformatic analysis predicted a putative binding site of miR-363 within the 3'-UTR of S1PR1 mRNA. Luciferase reporter assay showed that miR-363 directly targeted the 3'-UTR of S1PR1 mRNA. Transfection of miR-363 mimics suppressed S1PR1 expression in HCC cells, followed by the repression of the activation of ERK and STAT3. Moreover, we found that the expression of downstream genes of ERK and STAT3, including PDGF-A, PDGF-B, MCL-1 and Bcl-xL, was suppressed after miR-363 transfection. Taken together, the present study demonstrated that miR-363 was a negative regulator of S1PR1 expression in HCC cells and inhibited cell proliferation, suggesting that the miR-363/S1PR1 pathway might be a novel target for the treatment of HCC.
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http://dx.doi.org/10.1016/j.cellsig.2014.02.020DOI Listing
June 2014

PinX1, a novel target gene of p53, is suppressed by HPV16 E6 in cervical cancer cells.

Biochim Biophys Acta 2014 Feb 8;1839(2):88-96. Epub 2014 Jan 8.

Department of Obstetrics and Gynecology, Daping Hospital, Research Institute of Surgery, Third Military Medical University, Chongqing 400042, China. Electronic address:

The aberrant activation of telomerase is critical for the initiation and development of human cervical cancer, which is dependent on the activation of human telomerase reverse transcriptase (hTERT). Recently, Pin2/TRF1-interacting protein X1 (PinX1) has been identified as a suppressor of hTERT. It has been found that the telomerase is activated while the level of PinX1 is decreased in cervical cancer. However, the regulatory mechanism of PinX1 in cervical cancer cells remains unclear. In the present study, we demonstrated that the level of PinX1 is regulated by p53, and p53 functions as a transcriptional factor to directly activate the expression of PinX1 in cervical cancer cells. Moreover, we found that HPV16 E6 suppresses the expression of PinX1 via inhibiting p53 transcriptional activity, resulting in the enhancement of telomerase activity. This study not only for the first time shows that PinX1 is a novel target gene of p53 but also suggests that suppression of p53/PinX1 pathway may be a novel mechanism by which HPV16 E6 enhances the telomerase activity in cervical cancer cells.
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http://dx.doi.org/10.1016/j.bbagrm.2014.01.004DOI Listing
February 2014

MicroRNA-1 and microRNA-206 suppress LXRα-induced lipogenesis in hepatocytes.

Cell Signal 2013 Jun 14;25(6):1429-37. Epub 2013 Mar 14.

Department of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Third Military Medical University, Chongqing 400038, China.

Liver X receptor α (LXRα) plays a critical role in the transcriptional control of lipid metabolism. LXR activation induces the expression of lipogenic genes, which promote hepatic steatosis and steatohepatitis. However, the regulation of LXR is not fully understood. MicroRNAs (miRs) are regarded as important negative regulators of gene expression. In this study, we found that miR-1/miR-206 repressed LXRα-induced accumulation of lipid droplets in hepatocytes. In addition, bioinformatic analysis predicted a same putative target-site for miR-1/miR-206 located within the 3'-untranslated region (3'-UTR) of LXRα mRNA. The reporter assay revealed that miR-1/miR-206 directly targeted the 3'-UTR of LXRα mRNA. Furthermore, miR-1/miR-206 repressed LXRα expression at both mRNA and protein levels, accompanied with the inhibition of expression of LXRα target genes, such as sterol-regulatory element binding protein 1c, fatty acid synthase, carbohydrate responsive element-binding protein and acetyl-CoA carboxylase 1, which are important effectors of LXRα implicated in lipogenesis. Moreover, ectopic expression of LXRα without the 3'-UTR dramatically attenuated the miR-1/miR-206-induced decrease of lipogenic genes and lipid droplet accumulation. Taken together, we for the first time demonstrated that miR-1/miR-206 attenuated LXRα-induced lipogenesis by targeting the 3'-UTR of LXRα mRNA, suggesting that miR-1/miR-206-LXRα pathway may be a novel target for the treatment of lipogenesis-associated diseases.
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http://dx.doi.org/10.1016/j.cellsig.2013.03.003DOI Listing
June 2013

Activation of liver X receptor attenuates endothelin-1 expression in vascular endothelial cells.

Int J Biochem Cell Biol 2012 Dec 24;44(12):2299-307. Epub 2012 Sep 24.

Department of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Third Military Medical University, Chongqing 400038, PR China.

Endothelin-1 (ET-1), predominantly produced by vascular endothelial cells (VECs), plays an important role in the pathogenesis of inflammatory diseases. Liver X receptor (LXR), a typical nuclear receptor, is known for inhibiting expression of inflammatory molecules. However, it remains unclear whether LXR suppresses ET-1 expression. In the present study, we showed that pretreatment with GW3965, a specific ligand of LXR, significantly attenuated lipopolysaccharide (LPS)-induced ET-1 in mice plasma. The in vitro experiments showed that both LXRα and β were expressed in human VECs, and they are functional as demonstrated by induction of the target gene ABCA1 after treatment with GW3965. Moreover, activation of LXR with GW3965 in human VECs dramatically attenuated the basal and LPS-stimulated ET-1 production at both transcriptional and translational levels. Luciferase reporter assays indicated that LXR activation suppressed the transcriptional activity of the human ET-1 gene promoter, and repressed the activity of a heterologous promoter driven by the response elements of activator-1 (AP-1) or nuclear factor-κB (NF-κB). Electrophoretic mobility shift and chromatin immunoprecipitation assays showed that activation of LXR reduced the binding of the transcriptional factors AP-1 and NF-κB to the ET-1 gene promoter region. In conclusion, activation of LXR represses ET-1 expression in vivo and in vitro, which may be involved in the negatively interfering with AP-1/NF-κB signaling. These results suggest that LXRs may serve as a novel molecular target for modulating ET-1 expression in VECs, and even for the treatment of ET-1-associated inflammatory diseases.
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http://dx.doi.org/10.1016/j.biocel.2012.09.010DOI Listing
December 2012

Functional identification of the DNA packaging terminase from Pseudomonas aeruginosa phage PaP3.

Arch Virol 2012 Nov 22;157(11):2133-41. Epub 2012 Jul 22.

Department of Microbiology, Third Military Medical University, Chongqing, China.

Terminase proteins are responsible for DNA recognition and initiation of DNA packaging in phages. We previously reported the genomic sequence of a temperate Pseudomonas aeruginosa phage, PaP3, and determined its precise integration site in the host bacterial chromosome. In this study, we present a detailed functional identification of the DNA packaging terminase for phage PaP3. The purified large subunit p03 was demonstrated to possess ATPase and nuclease activities, as well as the ability to bind to specific DNA when it is unassembled. In addition, a small terminase subunit (p01) of a new type was found and shown to bind specifically to cos-containing DNA and stimulate the cos-cleavage and ATPase activities of p03. The results presented here suggest that PaP3 utilizes a typical cos site mechanism for DNA packaging and provide a first step towards understanding the molecular mechanism of the PaP3 DNA packaging reaction.
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http://dx.doi.org/10.1007/s00705-012-1409-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3488191PMC
November 2012

Activation of farnesoid X receptor increases the expression of cytokine inducible SH2-containing protein in HepG2 cells.

J Interferon Cytokine Res 2012 Nov 20;32(11):517-23. Epub 2012 Jul 20.

Department of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Third Military Medical University, Chongqing, People's Republic of China.

Cytokine inducible SH2-containing protein (CISH), which negatively regulates cytokine signaling by inhibiting JAK2/STAT5 activity, is regarded as a therapeutic target for inflammatory diseases. Farnesoid X receptor (FXR), a ligand-activated transcription factor, has been proposed to play a protective function in the inflammatory responses. However, the role of FXR in modulation of CISH expression is unknown. In the present study, we for the first time identified that in human hepatoma cell line HepG2 the activation of FXR by the natural agonist chenodeoxycholic acid (CDCA) and the synthetic specific agonist GW4064 upregulated CISH at both transcriptional and translational levels, and inhibited interleukin (IL)6-induced STAT5 activation. Moreover, the in vivo experiment demonstrated that gavaging mice with CDCA increased CISH expression and reduced basal STAT5 phosphorylation in liver tissues. Reporter assay showed that FXR agonists enhanced the transcriptional activity of CISH promoter. These data suggest that FXR may serve as a novel molecular target for manipulating CISH expression in hepatocytes. FXR-mediated upregulation of CISH may play an important role in the homeostasis of cytokine signal networks and be beneficial to control cytokine-associated inflammatory diseases.
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http://dx.doi.org/10.1089/jir.2012.0008DOI Listing
November 2012

FXR ligands protect against hepatocellular inflammation via SOCS3 induction.

Cell Signal 2012 Aug 25;24(8):1658-64. Epub 2012 Apr 25.

Department of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Third Military Medical University, Chongqing 400038, China.

Because of the anti-inflammatory actions of farnesoid X receptor (FXR) agonists, FXR has received much attention as a potential therapeutic target. However, the molecular mechanisms of actions have not yet been elucidated. In the present study, we reported that in the animal model of LPS-induced liver injury, administration of the FXR natural ligand CDCA could attenuate hepatocyte inflammatory damage, reduce transaminase activities, suppress inflammation mediators (IL-6, TNF-α and ICAM-1) expression and inhibit STAT3 phosphorylation. These protective effects of FXR were accompanied by an increased expression of suppressor of cytokine signaling 3 (SOCS3), which is a negative feedback regulator of cytokine-STAT3 signaling. We then demonstrated that the beneficial effects of FXR agonist in STAT3 activation were weakened by small interfering RNA-mediated SOCS3 knockdown in hepacytes. Moreover we observed both natural ligand CDCA and synthetic ligand GW4064 could upregulate SOCS 3 expression by enhancing the promoter activity in hepatocytes. These results suggest modulation of SOCS3 expression may represent a novel mechanism through which FXR activation could selectively affect cytokine bioactivity in inflammation response. FXR ligands may be potentially therapeutic in the treatment of liver inflammatory diseases via SOCS3 induction.
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http://dx.doi.org/10.1016/j.cellsig.2012.04.015DOI Listing
August 2012

Downregulation of human farnesoid X receptor by miR-421 promotes proliferation and migration of hepatocellular carcinoma cells.

Mol Cancer Res 2012 Apr 23;10(4):516-22. Epub 2012 Mar 23.

Department of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Third Military Medical University, Chongqing 400038, China.

The farnesoid X receptor (FXR) is a member of the nuclear receptor superfamily that is highly expressed in liver, kidney, adrenal gland, and intestine. It plays an important role in regulating the progression of several cancers including hepatocellular carcinoma (HCC). So it is necessary to study the regulation of FXR. In this study, we found that the expression of miR-421 was inversely correlated with FXR protein level in HCC cell lines. Treatment with miR-421 mimic repressed FXR translation. The reporter assay revealed that miR-421 targeted 3' untranslated region of human FXR mRNA. Furthermore, downregulation of FXR by miR-421 promoted the proliferation, migration, and invasion of HCC cells. These results suggest that miR-421 may serve as a novel molecular target for manipulating FXR expression in hepatocyte and for the treatment of HCC.
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http://dx.doi.org/10.1158/1541-7786.MCR-11-0473DOI Listing
April 2012

Peroxisome proliferator-activated receptor γ agonist troglitazone inhibits high mobility group box 1 expression in endothelial cells via suppressing transcriptional activity of nuclear factor κB and activator protein 1.

Shock 2011 Sep;36(3):228-34

Department of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Daping Hospital and Research Institute of Surgery, Third Military Medical University, Chongqing, PR China.

High mobility group box 1 (HMGB1), a delayed mediator of proinflammatory cytokines, could initiate and amplify inflammatory responses to infection, injury, and other inflammatory stimuli, and it has emerged as a potential therapeutic target for inflammatory diseases. The overexpression of HMGB1 in endothelial cells has been proved to contribute to the development of these diseases. Because many proinflammatory cytokines expression were suppressed by thiazolidinediones (TZDs), agonists for nuclear receptor peroxisome proliferator-activated receptor γ (PPARγ), whether TZDs can inhibit HMGB1 expression and function is of great interest, however, it remains unknown. Herein, we provide evidence that PPARγ agonist troglitazone, a member of the TZD class, modulates HMGB1 expression in the endothelial cell line EA.hy926 and propose a potential mechanism for that. Results from polymerase chain reaction experiments revealed that PPARγ is expressed in EA.hy926 cells, and it can be activated by troglitazone. Troglitazone inhibited the basal and LPS-stimulated HMGB1 expression at the mRNA level and protein level. A luciferase reporter assay showed that troglitazone inhibited not only the transcriptional activation of the HMGB1 promoter but also activities of heterologous promoters driven by nuclear factor κB (NF-κB) or activator protein 1 (AP-1) response elements. Altogether, these data suggest that NF-κB and AP-1 may participate in the inhibitory effect on HMGB1 transcription induced by troglitazone. Activation of PPARγ by troglitazone is effective for HMGB1 inhibition via suppressing NF-κB and AP-1 transcriptional activity in endothelial cells, which provides a new potential strategy to suppress excessive HMGB1 in inflammatory diseases.
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http://dx.doi.org/10.1097/SHK.0b013e318225b29aDOI Listing
September 2011

Immunolocalization of protein C inhibitor in differentiation of human epidermal keratinocytes.

Acta Histochem 2007 15;109(6):461-7. Epub 2007 Aug 15.

Department of Cell Biology, The Third Military Medical University, Chongqing 400038, People's Republic of China.

Keratinocytes propagated in low calcium (0.05 mM) serum-free medium grow as monolayers and exhibit morphological and biosynthetic phenotypes similar to the keratinocytes of the basal layer in normal epidermis. When the calcium in the medium is increased to 1.5 mM, the keratinocytes start to stratify and differentiate. Such differentiation is important in the formation of an epidermal barrier. Proteolysis plays a crucial role in the process. The functions of most of the plasminogen activator cascade components in human skin have been studied, but little was known about the expression and role of protein C inhibitor in the differentiation of human epidermal keratinocytes. In the present study, we used immunohistochemistry and immunocytochemistry to examine the immunolocalization of protein C inhibitor in normal human skin and in cultured keratinocytes in serum-free medium with low and high calcium, respectively. The results indicated that protein C inhibitor is mainly localized in superficial and more differentiated keratinocytes in normal human epidermis. Keratinocytes positive for protein C inhibitor were detected in cultures containing both low and high calcium media, and the level of protein C inhibitor was increased in high calcium medium. This increase was accompanied by an altered intracellular distribution, from the perinuclear cytoplasm in undifferentiated keratinocytes to the whole cytoplasm in differentiated keratinocytes. Further study revealed that protein C inhibitor was incorporated into the cornified envelope in normal skin keratinocytes and cultured differentiated keratinocytes. Our results suggest that protein C inhibitor may be involved in the differentiation of keratinocytes.
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http://dx.doi.org/10.1016/j.acthis.2007.04.007DOI Listing
February 2008

The expression patterns of vascular endothelial growth factor and thrombospondin 2 after corneal alkali burn.

Colloids Surf B Biointerfaces 2007 Oct 17;60(1):105-9. Epub 2007 Jun 17.

State Key Laboratory of Trauma, Burns and Combined Injury, Research Institute for Traffic Medicine, Chongqing Key Laboratory of Vehicle/Biological Crash Security, Third Military Medical University, Chongqing 400042, China.

The aim of the investigation was to explore the expression patterns of VEGF and TSP2 after corneal alkali burn in vivo. After the model of corneal alkali burn was established in mice, the expression levels of VEGF and TSP2 were determined by immunohistochemistry (IHC), RT-PCR, image analysis and statistical evaluation. Compared with control group, the expression level of VEGF increased significantly at 6h after alkali burn and reached its maximum at 12h. Then, it increased again till the second peak appeared at 96h and 192h. The VEGF-positive reaction mainly gathered in the stroma of cornea. On the other hand, the expression of TSP2 enhanced at 3h and attained two peaks at 6h and 96h, respectively, with the process of wound healing. TSP2 was expressed mainly in the base of epithelial layer. The expression patterns of VEGF and TSP2 reflect the complicated interaction with many factors including promoted and inhibited vascularization in vivo. Moreover, it might provide a novel method for controlling vascular hyperplasia in future clinical work according to the data of VEGF and TSP2.
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http://dx.doi.org/10.1016/j.colsurfb.2007.06.013DOI Listing
October 2007

A bio-mathematical model of time prediction in corneal angiogenesis after alkali burn.

Burns 2007 Jun 9;33(4):511-7. Epub 2007 Mar 9.

State Key Laboratory of Trauma, Burns and Combined Injury, Research Institute for Traffic Medicine, Department 4, Institute of Surgery Research, Daping Hospital, Third Military Medical University, Chongqing, PR China.

Background: The determination of angiogenesis time is the key prerequisite to obtaining a balance between valid repair and excessive angiogenesis in wound healing. The aim of the investigation was to establish a bio-mathematical model predicting corneal angiogenesis time after alkali burn by back propagation neural network (BP neural network).

Methods: The corneas of mice in 24 groups were burned by 0.01 mol/l NaOH. Five mice in each group were sacrificed at 6h after alkali burn. The expression levels of vegf and tsp2, determined by real-time quantitive PCR, were used as input vectors in BP neural network. Meanwhile, the corneal angiogenesis of other mice, inspected every 3h in 24 groups till the angiogenesis time were determined, served as output vectors. The data of 18 groups were randomly chosen for network adaptation while that of other 6 groups for simulation forecasting with functions of minmax (), postreg, prepca, trapca, respectively.

Results: A bio-mathematical model of two-level BP neural network was established, for its purpose to predict the angiogenesis time through the expression values of vegf and tsp2. The performance index (0.00999996) was smaller than the target value (0.01) after adapting 36,557 times and the accuracy rate of this predict system was 83.33%. Furthermore, the ideal regression line and the optimization regression line were almost coincident (R=0.988 in network adaptation and R=0.793 in simulation forecasting).

Conclusions: The investigation indicated that the bio-mathematical model had available performance of simulation and forecasting. It might provide a novel method to solve clinical problems.
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http://dx.doi.org/10.1016/j.burns.2006.08.029DOI Listing
June 2007

Bulge cells of human hair follicles: segregation, cultivation and properties.

Colloids Surf B Biointerfaces 2006 Jan 4;47(1):50-6. Epub 2006 Jan 4.

Department of Cell Biology, Third Military Medical University, Chongqing 400038, PR China.

The bulge region of hair follicle has been reported as a putative reservoir of hair follicle stem cell (HFSC) for years; however, few studies were done about the characteristics of bulge-originated cells in vitro up to now. In this experiment, the bulge cells isolated from human hair follicles by enzymatic digestion and microdissection were cultured and passaged, and the morphological and biological features of cultured bulge cells were investigated by microscopy and immunocytochemistry. The result showed that new-proliferated cells could be observed on the second day after inoculation, and the quantity of the cells with a greater proliferation potential, reached a peak at the 6th day and maintained this higher level for several days. The mitotic figures of bulge cells were seen and these cells showed undifferentiated morphologic features. The bulge cells strongly expressed K19 and beta1-integrin, which are the markers of HFSC, in a descensive way with the culture time. The result indicates that the cultured bulge cell from human hair follicle possesses the properties of primitive cells and supports the hypothesis that HFSC resides in the bulge area.
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http://dx.doi.org/10.1016/j.colsurfb.2005.11.017DOI Listing
January 2006

Patterns of nestin expression in human skin.

Cell Biol Int 2006 Feb 7;30(2):144-8. Epub 2005 Nov 7.

Department of Cell Biology, The Third Military Medical University, Chong Qing 400038, PR China.

Nestin, a member of the sixth class of intermediate filament proteins, has long been known not only as a specific marker for central nervous system stem cells, but also as an indicator of the degree of neural stem cell differentiation. Immunohistochemical analysis showed nestin expression in the epidermis and the upper two-third of the hair follicle in non-balding human scalp skin, but not in the lower third of the follicle. Expression was very weak in the sebaceous gland. The level of nestin mRNA transcription was much higher in the bulge region of the follicle than in the sebaceous gland. These results show that the pattern of nestin expression is related to the differentiation of epidermal stem cells.
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http://dx.doi.org/10.1016/j.cellbi.2005.09.005DOI Listing
February 2006

Changes of uPA and uPA-R expression in the cornea after alkali burn.

Colloids Surf B Biointerfaces 2004 Aug;37(1-2):49-52

Department of Cell Biology, Third Military Medical University, Chongqing 400038, PR China.

Purpose: To investigate the expression levels of uPA and uPA-R in corneal repair after alkali burn.

Methods: The corneal alkali burn models were established in vitro and in vivo, then immunocytochemistry (ICC) of uPA/uPA-R and image analysis and statistical evaluation were performed to determine their expression levels both in vitro and in vivo.

Results: Compared with control group, the expressions of uPA and uPA-R after alkali burn had no significant increases till 6h, then increased rapidly from 12h to 24h and reached their maxima at 24h. From 24h, their expression levels decreased rapidly. In vivo, they rebounded again after 48h and attained their second peaks at 96h, respectively. After that, their expressions decreased again. The uPA-positive reaction mainly distributed in the cytoplasm while that of uPA-R mostly distributed on the cellular membrane. Their expression changes were similar to each other, both in vivo and in vitro. In vivo, uPA and uPA-R expressed and gathered in the basal layer of corneal epithelium.

Conclusions: These results suggest that the time phase of 24h after wound is the typical stage associating with the expressional maximum of uPA and uPA-R both in vivo and in vitro. Furthermore, the results also imply that the expression changes of uPA and uPA-R correlate to the wound healing after the corneal alkali burn, uPA and uPA-R coordinate with each other to stimulate the wound healing.
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http://dx.doi.org/10.1016/j.colsurfb.2004.05.018DOI Listing
August 2004
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