Publications by authors named "Hainan Li"

14 Publications

  • Page 1 of 1

Selective laser sintering versus conventional lost-wax casting for single metal copings: A systematic review and meta-analysis.

J Prosthet Dent 2021 Mar 29. Epub 2021 Mar 29.

Assistant, Department of Restorative Dentistry, Stomatological Hospital of Chongqing Medical University, Chongqing Key Laboratory of Oral Diseases and Biomedical Sciences, Chongqing Municipal Key Laboratory of Oral Biomedical Engineering of Higher Education, Chongqing, PR China.

Statement Of Problem: Evidence comparing the marginal and internal fit of single metal copings fabricated via selective laser sintering and conventional lost-wax casting is inadequate.

Purpose: The purpose of this systematic review was to compare the fit of single metal copings fabricated via selective laser sintering and lost-wax casting. Moreover, the effects of different variables on fit accuracy were determined.

Material And Methods: Google Scholar, ScienceDirect, SpringerLink, and Wiley databases were searched electronically as well as manually. The mean absolute marginal gap, marginal gap, internal gap, axial gap, and occlusal gap values of single metal copings fabricated via selective laser sintering and lost-wax casting were statistically analyzed to determine and evaluate the factors affecting the fit accuracy (α=.05).

Results: Single metal copings fabricated via selective laser sintering had mean absolute marginal gaps and occlusal gaps similar to those of copings fabricated via lost-wax casting, based on a subgroup meta-analysis of gaps evaluated using stereomicroscopy (P>.05). The fit of single metal copings was not affected by the type of tooth (P>.05). The conventional impression, the indirect digital scan, and the direct digital scan led to similar values of mean axial gap, internal gap, and marginal gap for the copings fabricated via lost-wax casting (P>.05). The indirect and direct digital scans led to similar values of mean axial gap, internal gap, and marginal gap for the copings fabricated via selective laser sintering (P>.05). Printed wax patterns provided significantly smaller mean axial gap values than milled plastic or milled wax patterns for the copings fabricated via lost-wax casting (P<.05). Printed, milled, and conventional wax patterns had similar mean marginal gaps and internal gaps for the copings fabricated via lost-wax casting (P>.05). For single copings fabricated via lost-wax casting, Ni-Cr and Co-Cr had similar mean internal gaps (P>.05).

Conclusions: No statistically significant differences were found between single metal copings fabricated via selective laser sintering and lost-wax casting. Selective laser sintering can satisfy the clinical requirement for single metal copings.
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http://dx.doi.org/10.1016/j.prosdent.2021.02.011DOI Listing
March 2021

Genomic Profiling Identified Novel Prognostic Biomarkers in Chinese Midline Glioma Patients.

Front Oncol 2020 3;10:607429. Epub 2021 Mar 3.

Department of Pathology, Guangdong Provincial People's Hospital, Guangzhou, China.

Background: Molecular characteristics are essential for the classification and grading of gliomas. However, diagnostic classification of midline glioma is still debatable and substantial molecular and clinical heterogeneity within each subgroup suggested that they should be further stratified. Here, we studied the mutation landscape of Chinese midline glioma patients in hope to provide new insights for glioma prognosis and treatment.

Methods: Tissue samples from 112 midline glioma patients underwent next-generation sequencing targeting 425 cancer-relevant genes. Gene mutations and copy number variations were investigated for their somatic interactions and prognostic effect using overall survival data. Pathway-based survival analysis was performed for ten canonical oncogenic pathways.

Results: We identified several currently established diagnostic and prognostic biomarkers of glioma, including (33%), (26%), (24%), (21%), (14%) (14%), (13%), and (6%). Among all genetic aberrations with more than 5% occurrence rate, six mutations and three copy number gains were greatly associated with poor overall survival (univariate, P < 0.1). Of these, mutations (hazard ratio [HR], 3.00; 95% confidence interval [CI], 1.37-6.61; P = 0.01) and mutations (HR, 2.04; 95% CI, 1.08-3.84; P = 0.02) remained significant in multivariate analyses. Additionally, we have also identified a novel amplification (found in 31% patients) as a potential independent biomarker for glioma (multivariate HR, 2.78; 95% CI, 1.53-5.08; P < 0.001), which was seldom reported in public databases. Pathway analyses revealed significantly worse prognosis with abnormal PI3K (HR, 1.81; 95% CI, 1.12-2.95; P = 0.01) and cell cycle pathways (HR, 1.97; 95% CI, 1.15-3.37; P = 0.01), both of which stayed meaningful after multivariate adjustment.

Conclusions: In this study, we discovered shorter survival in midline glioma patients with PIK3CA and TERT mutations and with abnormal PI3K and cell cycle pathways. We also revealed a novel prognostic marker, amplification that collectively provided new insights and opportunities in understanding and treating midline gliomas.
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http://dx.doi.org/10.3389/fonc.2020.607429DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7968371PMC
March 2021

Increased M1 Macrophages Infiltration Correlated With Poor Survival Outcomes and Radiation Response in Gliomas.

Dose Response 2020 Oct-Dec;18(4):1559325820964991. Epub 2020 Oct 16.

Department of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, China.

Background: Gliomas are the malignance of a poor prognosis. The current WHO classification remains unable to predict survival outcomes accurately. Novel surrogates are highly required for improved stratification of patients and hence, allowing to delivery of the most appropriate treatment.

Methods: Transcriptional profiles of 301 glioma cases on the platform of Chinese Glioma Genome Atlas (CGGA) were retrospectively studied.

Results: Extracellular matrix (ECM) scores were established by integrating a panel of most featured gene-signatures, correlating well with pathological tumor stages. Linear regression analysis revealed that the ECM score corroborated with the infiltration status of monocytes, M0 and M1 macrophages. Furthermore, the WHO stage II-IV dependent abundance of those 3 immune cells was determined. Univariate and multivariate analysis of clinicopathological characteristics in the GBM cohort identified M1 enrichment score as an independent risk factor. A high abundance of M1 macrophages was associated with poor survival outcomes and radiotherapy response in IDH-wildtype GBM.

Conclusions: Our study demonstrated that M1 macrophages correlated with WHO grades and predicted robustly for the survival performance for GBM patients. Increased infiltration of M1 macrophages was associated with a poor radiation response for IDH-wildtype GBM. Together, it will facilitate more precise stratifications of glioma patients based on molecular and immunological surrogates.
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http://dx.doi.org/10.1177/1559325820964991DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7573741PMC
October 2020

Preparation and In Vitro and In Vivo Antitumor Effects of VEGF Targeting Micelles.

Technol Cancer Res Treat 2020 Jan-Dec;19:1533033820957022

154454The Second Hospital of Jilin University, Nanguan District, Changchun, China.

Background: Doxorubicin (DOX) has antitumor effects mediated by cell viability inhibition and by inducing cellular apoptosis. However, it has limited use in clinical applications due to various factors such as hydrophobicity, dose-dependent toxicity effects on normal tissues, short cycle retention time, and low targeting ability. This study aims at enhancing hydrophilicity of DOX to restrict its toxic effects to within or around the tumor sites and also to improve its targeting ability to enhance antitumor efficiency.

Methods: Micelles composed of biodegradable poly (ethylene glycol)-poly (lactic acid) copolymers (PEG-PLA) were employed to deliver DOX via a self-assembly method and were coupled to VEGF antibodies. The morphology, size, and physical stability of PEG-PLA-DOX targeting VEGF micelles (VEGF-PEG-PLA-DOX micelles) were assessed. Then, the release ability of DOX from these micelles was monitored, and their drug loading capacity was calculated. MTT assay revealed the antitumor effect of VEGF-PEG-PLA-DOX micelles. Moreover, ROS release was measured to evaluate apoptotic effects of these nanoparticle micelles. therapeutic efficiencies of VEGF-PEG-PLA-DOX micelles on a lung cancer nude mouse model was evaluated.

Results: DOX-loaded micelles were obtained with a drug loading capacity of 12.2% and were monodisperse with 220 nm average diameter and a controlled DOX release for extended periods. In addition, VEGF-PEG-PLA-DOX micelles displayed a larger cell viability inhibitory effect as measured via MTT assays and greater cell apoptosis induction through ROS levels compared with PEG-PLA-DOX micelles or free DOX. Furthermore, VEGF-PEG-PLA-DOX micelles could improve antitumor effects of DOX by reducing tumor volume and weight.

Conclusions: VEGF-PEG-PLA-DOX micelles displayed a larger anti-tumor effect both in A549 cells and in an lung cancer nude mouse model compared with PEG-PLA-DOX micelles or free DOX, and hence they have potential clinical applications in human lung cancer therapy.
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http://dx.doi.org/10.1177/1533033820957022DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7488921PMC
September 2020

Cooperation and Competition among information on social networks.

Sci Rep 2020 07 22;10(1):12160. Epub 2020 Jul 22.

College of Science, Huazhong Agricultural University, Wuhan, 430070, China.

When multiple information are spread on social networks, there may be Cooperation and Competition among these information. Based on a new spreading model of multiple information, we studied Cooperation and Competition in information spreading, and analyzed the influence of different factors on Cooperation and Competition. Through a large number of computer simulation experiments, we found that: (1) when multiple information are spread on social networks, there is Cooperation and Competition among these information; (2) the smaller the distance between two information sources is, the stronger the Cooperation and Competition among these information are; (3) the greater the value of social reinforcement is, the stronger the Cooperation and Competition among these information are; (4) the weaker the human heterogeneity of one information is, the stronger the Cooperation and Competition among this information and other information are.
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http://dx.doi.org/10.1038/s41598-020-69098-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7376155PMC
July 2020

Downregulation of hyperpolarization-activated cyclic nucleotide-gated channels (HCN) in the hippocampus of patients with medial temporal lobe epilepsy and hippocampal sclerosis (MTLE-HS).

Hippocampus 2020 Oct 16;30(10):1112-1126. Epub 2020 Jun 16.

Department of Neurology, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, China.

Changes in the expression of HCN ion channels leading to changes in I function and neuronal excitability are considered to be possible mechanisms involved in epileptogenesis in kinds of human epilepsy. In previous animal studies of febrile seizures and temporal lobe epilepsy, changes in the expression of HCN1 and HCN2 channels at different time points and in different parts of the brain were not consistent, suggesting that transcriptional disorders involving HCNs play a crucial role in the epileptogenic process. Therefore, we aimed to assess the transcriptional regulation of HCN channels in Medial temporal lobe epilepsy with hippocampal sclerosis (MTLE-HS) patients. This study included eight nonhippocampal sclerosis patients and 40 MTLE-HS patients. The mRNA expression of HCN channels was evaluated by qRT-PCR, while the protein expression was quantitatively analyzed by Western blotting. The subcellular localization of HCN channels in the hippocampus was explored by immunofluorescence. We demonstrated that the mRNA and protein expression of HCN1 and HCN2 are downregulated in controls compared to that in MTLE-HS patients. In the hippocampal CA1/CA4 subregion and GCL, in addition to a large decrease in neurons, the expression of HCN1 and HCN2 on neuronal cell membranes was also downregulated in MTLE-HS patients. These findings suggest that the expression of HCN channels are downregulated in MTLE-HS, which indicates that the decline in HCN channels in the hippocampus during chronic epilepsy in MTLE-HS patients leads to the downregulation of I current density and function, thereby reducing the inhibitory effect and increasing neuronal excitability and eventually causing disturbances in the electrical activity of neurons.
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http://dx.doi.org/10.1002/hipo.23219DOI Listing
October 2020

Insulin Signal Transduction is Impaired in the Type 2 Diabetic Retina.

J Diabetes Clin Res 2020 25;2(1):12-15. Epub 2020 Mar 25.

Department of Ophthalmology, Visual, and Anatomical Sciences, Wayne State University, Detroit, MI USA.

Rates of type 2 diabetes are reaching epidemic levels. Yet, the tissue specific alterations due to insulin resistance are only recently being investigated. The goal of the present study was to evaluate retinal insulin signal transduction in a common mouse model of type 2 diabetes, the db/db mouse. Retinal lysates from five month old male db/db and db/+ (control) mice were collected and processed for Western blotting or ELISA analyses for insulin receptor, insulin receptor substrate-1 (IRS-1), Akt, tumor necrosis factor alpha (TNFα) and caspase 3 levels. Data demonstrate increased TNFα and IRS-1 phosphorylation on serine 307. This led to decreased Akt phosphorylation on serine 473 and increased cleavage of caspase 3. Taken together, the data suggest dysfunctional insulin signaling in the retina of the db/db mouse. insulin.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7236787PMC
March 2020

RELA Fusion in Supratentorial Extraventricular Ependymomas: A Morphologic, Immunohistochemical, and Molecular Study of 43 Cases.

Am J Surg Pathol 2019 12;43(12):1674-1681

Departments of Pathology.

Supratentorial extraventricular ependymomas (STEEs) are relatively rare ependymomas, and their pathologic and genetic characteristics are still poorly understood. The aim of this study was to determine the histologic, immunohistochemical, and RELA fusion features, as well as to clarify in more detail the clinical courses of STEEs. Data from a total of 43 patients with STEEs was analyzed retrospectively. The status of RELA fusion was evaluated using fluorescence in situ hybridization. The expression levels of L1CAM, p65, cyclin D1, and p53 were assessed using immunohistochemistry. Progression-free survival and overall survival were calculated via Kaplan-Meier estimation using the log-rank test. Among all 43 STEEs, 65.1% (28/43) are positive for RELA fusion. Interestingly, almost half of the patients with RELA fusion-positive ependymomas are adults (13/28), and 89.3% (25/28) cases are anaplastic ependymomas, which suggests that RELA fusion testing is necessary in adults with STEEs. We investigated the immunohistochemical status of p65, L1CAM and CCND1 protein expression for their ability to predict RELA fusion status. RELA fusion-positive STEEs are frequently associated with expression of p65 (85.2%), L1CAM (85.2%), and CCND1 (81.5%). The accuracy of predicting RELA fusion status was much higher when the expression of p65 and L1CAM was combined, that is, when both were immunopositive. The status of RELA fusion, p53 overexpression, and extent of tumor resection are significantly associated with prognosis.
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http://dx.doi.org/10.1097/PAS.0000000000001342DOI Listing
December 2019

Methylglyoxal triggers human aortic endothelial cell dysfunction via modulation of the K/MAPK pathway.

Am J Physiol Cell Physiol 2019 07 17;317(1):C68-C81. Epub 2019 Apr 17.

Department of Pharmaceutical Sciences, Eugene Applebaum College of Pharmacy and Health Sciences, Wayne State University , Detroit, Michigan.

Endothelial dysfunction is a key risk factor in diabetes-related multiorgan damage. Methylglyoxal (MGO), a highly reactive dicarbonyl generated primarily as a by-product of glycolysis, is increased in both type 1 and type 2 diabetic patients. MGO can rapidly bind with proteins, nucleic acids, and lipids, resulting in structural and functional changes. MGO can also form advanced glycation end products (AGEs). How MGO causes endothelial cell dysfunction, however, is not clear. Human aortic endothelial cells (HAECs) from healthy (H-HAECs) and type 2 diabetic (D-HAECs) donors were cultured in endothelial growth medium (EGM-2). D-HAECs demonstrated impaired network formation (on Matrigel) and proliferation (MTT assay), as well as increased apoptosis (caspase-3/7 activity and TUNEL staining), compared with H-HAECs. High glucose (25 mM) or AGEs (200 ng/ml) did not induce such immediate, detrimental effects as MGO (10 µM). H-HAECs were treated with MGO (10 µM) for 24 h with or without the ATP-sensitive potassium (K) channel antagonist glibenclamide (1 µM). MGO significantly impaired H-HAEC network formation and proliferation and induced cell apoptosis, which was reversed by glibenclamide. Furthermore, siRNA against the K channel protein Kir6.1 significantly inhibited endothelial cell function at basal status but rescued impaired endothelial cell function upon MGO exposure. Meanwhile, activation of MAPK pathways p38 kinase, c-Jun NH-terminal kinase (JNK), and extracellular signal-regulated kinase (ERK) (determined by Western blot analyses of their phosphorylated forms, p-JNK, p-p38, and p-ERK) in D-HAECs were significantly enhanced compared with those in H-HAECs. MGO exposure enhanced the activation of all three MAPK pathways in H-HAECs, whereas glibenclamide reversed the activation of p-stress-activated protein kinase/JNK induced by MGO. Glyoxalase-1 (GLO1) is the endogenous MGO-detoxifying enzyme. In healthy mice that received an inhibitor of GLO1, MGO deposition in aortic wall was enhanced and endothelial cell sprouting from isolated aortic segment was significantly inhibited. Our data suggest that MGO triggers endothelial cell dysfunction by activating the JNK/p38 MAPK pathway. This effect arises partly through activation of K channels. By understanding how MGO induces endothelial dysfunction, our study may provide useful information for developing MGO-targeted interventions to treat vascular disorders in diabetes.
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http://dx.doi.org/10.1152/ajpcell.00117.2018DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6689756PMC
July 2019

Ameliorating Methylglyoxal-Induced Progenitor Cell Dysfunction for Tissue Repair in Diabetes.

Diabetes 2019 06 18;68(6):1287-1302. Epub 2019 Mar 18.

Department of Pharmaceutical Sciences, Eugene Applebaum College of Pharmacy and Health Sciences, Wayne State University, Detroit, MI

Patient-derived progenitor cell (PC) dysfunction is severely impaired in diabetes, but the molecular triggers that contribute to mechanisms of PC dysfunction are not fully understood. Methylglyoxal (MGO) is one of the highly reactive dicarbonyl species formed during hyperglycemia. We hypothesized that the MGO scavenger glyoxalase 1 (GLO1) reverses bone marrow-derived PC (BMPC) dysfunction through augmenting the activity of an important endoplasmic reticulum stress sensor, inositol-requiring enzyme 1α (IRE1α), resulting in improved diabetic wound healing. BMPCs were isolated from adult male type 2 diabetic mice and their healthy corresponding control mice. MGO at the concentration of 10 µmol/L induced immediate and severe BMPC dysfunction, including impaired network formation, migration, and proliferation and increased apoptosis, which were rescued by adenovirus-mediated GLO1 overexpression. IRE1α expression and activation in BMPCs were significantly attenuated by MGO exposure but rescued by GLO1 overexpression. MGO can diminish IRE1α RNase activity by directly binding to IRE1α in vitro. In a diabetic mouse cutaneous wound model in vivo, cell therapies using diabetic cells with GLO1 overexpression remarkably accelerated wound closure by enhancing angiogenesis compared with diabetic control cell therapy. Augmenting tissue GLO1 expression by adenovirus-mediated gene transfer or with the small-molecule inducer trans-resveratrol and hesperetin formulation also improved wound closure and angiogenesis in diabetic mice. In conclusion, our data suggest that GLO1 rescues BMPC dysfunction and facilitates wound healing in diabetic animals, at least partly through preventing MGO-induced impairment of IRE1α expression and activity. Our results provide important knowledge for the development of novel therapeutic approaches targeting MGO to improve PC-mediated angiogenesis and tissue repair in diabetes.
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http://dx.doi.org/10.2337/db18-0933DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6610016PMC
June 2019

Disruption of GPR35 Exacerbates Dextran Sulfate Sodium-Induced Colitis in Mice.

Dig Dis Sci 2018 11 24;63(11):2910-2922. Epub 2018 Jul 24.

Department of Pharmaceutical Sciences, Eugene Applebaum College of Pharmacy and Health Sciences, Wayne State University, 259 Mack Ave, 3122 Applebaum Building, Detroit, MI, 48201, USA.

Background: G protein-coupled receptor 35 (GPR35) is an orphan receptor and is vastly expressed in immune cells and gastrointestinal cells, suggesting the potential physiological importance of GPR35 in these cells. Here, we tested the hypothesis that the lack of GPR35 expression in the colon mucosa exacerbates the severity of dextran sulfate sodium (DSS)-induced experimental colitis in mice.

Methods: Colitis was induced in GPR35 wild-type (GPR35) and GPR35 knockout (GPR35) mice through the administration of DSS in drinking water for 5 days followed by regular facility water for 1 day. Induction of colitis was evaluated by measuring relative body weight loss, clinical illness scores, and morphological changes in the colon. Abolition of Gpr35 gene expression in the colon mucosa of GPR35 mice was confirmed by quantitative real-time PCR (qPCR). Gene expressions of inflammatory and tissue remodeling cytokines were detected by qPCR. Human colorectal epithelial Caco cells were transfected with siRNA against GPR35 before treated with 1% DSS in vitro. Protein expressions were measured using Western blot.

Results: GPR35 mice receiving DSS showed a significantly worsened colitis disease with profound loss of body weight and a considerable amount of severe clinical illness compared to GPR35 mice that received DSS. The histology of colon sections from GPR35 mice showed extensive pathological changes including submucosal edema, diffuse ulcerations, and evidence of complete loss of crypts compared to wild-type mice. The mean histopathological score was significantly higher in GPR35 mice as compared to GPR35 mice. The qPCR data revealed significant expression of pro-inflammatory and tissue remodeling cytokines in GPR35 colon mucosa, including IL-1β, CXCL1, CXCL2, CCL2, HMGB1, TGFβ1, TGFβ3, MMP1/9/12. The protein expressions of Zonula occludens-1, E-cadherin, Claudin1 were decreased upon knocking down GPR35 with or without 1% DSS treatment.

Conclusions: Our experimental data suggest that lack of GPR35 resulted in worsened disease outcome in DSS-induced experimental colitis, indicating that GPR35 could play a crucial role in protecting from colonic inflammation and serve as a therapeutic target.
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http://dx.doi.org/10.1007/s10620-018-5216-zDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6373462PMC
November 2018

MiR-27b augments bone marrow progenitor cell survival via suppressing the mitochondrial apoptotic pathway in Type 2 diabetes.

Am J Physiol Endocrinol Metab 2017 10 11;313(4):E391-E401. Epub 2017 Jul 11.

Department of Pharmaceutical Sciences, Eugene Applebaum College of Pharmacy and Health Sciences, Wayne State University, Detroit, Michigan;

Bone marrow-derived progenitor cells (BMPCs) are potential candidates for autologous cell therapy in tissue repair and regeneration because of their high angiogenic potential. However, increased progenitor cell apoptosis in diabetes directly limits their success in the clinic. MicroRNAs are endogenous noncoding RNAs that regulate gene expression at the posttranscriptional level, but their roles in BMPC-mediated angiogenesis are incompletely understood. In the present study, we tested the hypothesis that the proangiogenic miR-27b inhibits BMPC apoptosis in Type 2 diabetes. Bone marrow-derived EPCs from adult male Type 2 diabetic mice and their normal littermates /+ mice were used. MiR-27b expression (real-time PCR) in EPCs was decreased after 24 h of exposure to methylglyoxal (MGO) or oxidized low-density lipoprotein but not high glucose, advanced glycation end products, the reactive oxygen species generator LY83583, or HO The increase in BMPC apoptosis in the diabetic mice was rescued following transfection with a miR-27b mimic, and the increased apoptosis induced by MGO was also rescued by the miR-27b mimic. p53 protein expression and the Bax/Bcl-2 ratio in EPCs (Western blot analyses) were significantly higher in mice, both of which were suppressed by miR-27b. Furthermore, mitochondrial respiration, as measured by oxygen consumption rate, was enhanced by miR-27b in diabetic BMPCs, with concomitant decrease of mitochondrial Bax/Bcl-2 ratio. The 3' UTR binding assays revealed that both Bax, and its activator RUNX1, were direct targets of miR-27b, suggesting that miR-27b inhibits Bax expression in both direct and indirect manners. miR-27b prevents EPC apoptosis in Type 2 diabetic mice, at least in part, by suppressing p53 and the Bax/Bcl-2 ratio. These findings may provide a mechanistic basis for rescuing BMPC dysfunction in diabetes for successful autologous cell therapy.
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http://dx.doi.org/10.1152/ajpendo.00073.2017DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5668595PMC
October 2017

An oligodeoxynucleotide with CCT repeats restrains CpG ODN-induced TLR9 trafficking.

Curr Pharm Biotechnol 2014 ;15(9):780-9

Department of Molecular Biology or Department of Immunology, College of Basic Medical Sciences, Jilin University, 126 N Xinmin Street, Changchun, Jilin 130021, China.

Toll-like receptor 9 (TLR9) can sense pathogen DNA and CpG ODN or even self-DNA by trafficking assisted by Unc93B1, an endoplasmic reticulum (ER) transmembrane protein, from ER to endolysosomes or cell surface. In previous study, we found that an oligodeoxynucleotide with CCT repeats (SAT05f) could selectively inhibit TLR7/9 activation. However, the mechanism for the inhibitory activity of SAT05f is still unknown. In present research, it was found that SAT05f could inhibit CpG ODN-induced the intracellular trafficking of TLR9 and Unc93B1 with feedback the responses of decreased surface TLR9 and enhanced TLR9 mRNA expression but not influence TLR9 protein level by using human plasmacytoid dendritic cell line CAL-1 cells, suggesting that SAT05f inhibits TLR9 activation by restraining TLR9 trafficking. Since the mitochondrial DNA released from injured tissue can cause systemic inflammatory response syndrome (SIRS), this study may provide valuable data for prevention and treatment of SIRS and rescue severe trauma patients.
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http://dx.doi.org/10.2174/1389201015666141031114708DOI Listing
August 2015