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Qiqihar, China

Gao B.,Harbin Medical University | Wang D.,First Hospital of Qiqihar | Sun W.,Harbin Medical University | Meng X.,Harbin Medical University | And 2 more authors.
Molecular Medicine Reports

Acute pancreatitis (AP) is a common acute digestive tract disease, with increased morbidity and mortality, and an unclear pathogenesis. Trypsinogen activation in pancreatic acinar cells may be the primary mechanism underlying the development of AP. Previous studies reported that autophagy participates in the formation of acinar cell vacuoles in AP and in the process of trypsinogen activation as an important cause of AP. Furthermore, microRNAs (miRNAs) maintain the autophagy process by regulating the expression of autophagy-associated genes. In the present study, an in vitro pancreatic acinar cell autophagy model was established using the AR42J starvation-induced pancreatic acinar cell line. Twenty differentially expressed microRNAs were identified using miRNA microarray. Bioinformatics analysis was used to predict the target genes of miRNAs and analyze the functions of differentially expressed miRNAs. The results demonstrated that only the downregulated miRNA rno-miR-148b-3p predicted 593 target genes with a statistical significance (P<.05), from which 10 genes were autophagy-associated. The results of gene ontology and pathway analyses demonstrated that the target genes of miRNAs were enriched in the Response to insulin stimulus, Regulation of cell death and the Insulin signaling pathways (P<.05, FDR<.05). In addition, protein-protein interaction network analysis demonstrated a widespread interaction among the 593 target genes. The results of the present study may provide novel targets for research on the mechanisms of autophagy-promoted AP and AP treatment. Source

Lu S.-k.,First Hospital of Qiqihar
Chinese Journal of Tissue Engineering Research

BACKGROUND: With rapid development of cell biology, molecular biology technique, and tissue engineering, increasing studies focus on seed cells for constructing skin wound surface by tissue engineering. OBJECTIVE: To summarize the biological characteristics of epidermal stem cells and investigate their regenerative and clinical application value in repair of skin wound surface. METHODS: A computer-based online retrieval of SNKI and PubMed database for searching papers describing epidermal stem cells for repair of skin injury using the key words of "epidermal stem cells, tissue engineering skin, wound surface" in English and Chinese. Papers related to research progress in epidermal stem cells for repair of skin injury were selected. Papers that were published recently in the same research field or in high-impact journals were selected. A total of 129 papers were initially retrieved. According to inclusion criteria, 25 papers were included for final analysis. RESULTS AND CONCLUSION: Epidermal stem cells support for epidermal generation, differentiation and wound healing. Epidermal stem cells provide the condition for maintaining skin normal structure and intracellular environment due to their normal proliferation and differentiation and are the ideal seed cells of skin tissue engineering. They show satisfactory prospects in treatment of large-area skin defects, cell therapy of skin disease, and gene therapy. In vitro culture of epidermal stem cells is a prerequisite for studying tissue engineering of artificial skin. As the isolation, purification and culture technology of epidermal stem cells continues to improve, we can quickly build epidermis. Nevertheless, application of epidermal stem cells requires further investigation. Source

Wu T.,Harbin Medical University | Wang X.,Harbin Medical University | Li J.,First Hospital of Qiqihar | Song X.,Frontier Corps Hospital in Heilongjiang Province | And 5 more authors.

Breast cancer is a highly heterogeneous disease that is clinically classified into several subtypes. Among these subtypes, basal-like breast cancer largely overlaps with triple-negative breast cancer (TNBC), and these two groups are generally studied together as a single entity. Differences in the molecular makeup of breast cancers can result in different treatment strategies and prognoses for patients with different breast cancer subtypes. Compared with other subtypes, basal-like and other ER+ breast cancer subtypes exhibit marked differences in etiologic factors, clinical characteristics and therapeutic potential. Anthracycline drugs are typically used as the first-line clinical treatment for basal-like breast cancer subtypes. However, certain patients develop drug resistance following chemotherapy, which can lead to disease relapse and death. Even among patients with basal-like breast cancer, there can be significant molecular differences, and it is difficult to identify specific drug resistance proteins in any given patient using conventional variance testing methods. Therefore, we designed a new method for identifying drug resistance genes. Subgroups, personalized biomarkers, and therapy targets were identified using cluster analysis of differentially expressed genes. We found that basal-like breast cancer could be further divided into at least four distinct subgroups, including two groups at risk for drug resistance and two groups characterized by sensitivity to pharmacotherapy. Based on functional differences among these subgroups, we identified nine biomarkers related to drug resistance: SYK, LCK, GAB2, PAWR, PPARG, MDFI, ZAP70, CIITA and ACTA1. Finally, based on the deviation scores of the examined pathways, 16 pathways were shown to exhibit varying degrees of abnormality in the various subgroups, indicating that patients with different subtypes of basal-like breast cancer can be characterized by differences in the functional status of these pathways. Therefore, these nine differentially expressed genes and their associated functional pathways should provide the basis for novel personalized clinical treatments of basal-like breast cancer. © 2015 Wu et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Source

Qi H.-P.,Harbin Medical University | Wang Y.,Harbin Medical University | Zhang Q.-H.,Harbin Medical University | Guo J.,Harbin Medical University | And 8 more authors.
Cellular Physiology and Biochemistry

Background/Aims: Cardiac remodeling is a common pathophysiological change along with chronic hypertension and myocardial infarction. Recent evidence indicated that cardiac tissue expressed peroxisome proliferator-activated receptor γ (PPARγ). However, the functional role of PPARγ in cardiac remodeling remained unclear. The present study was designed to investigate the relationship between PPARγ activation and pressure overload-induced cardiac remodeling. Methods: Cardiac remodeling model was successfully established by abdominal aorta ligation. Cardiac fibrosis and cardiomyocyte hypertrophy were simulated by 100 nM angiotensin II (Ang II) in vitro. Haemodynamic parameters, the expressions of Brg1, α-MHC, β-MHC, transforming growth factor beta 1 (TGF-β1), collagen-I, collagen-III and NF-κB were examined. Results: Morphological and haemodynamic measurements showed that the activation of PPARγ improved the impaired cardiac function and decreased interstitial fibrosis in cardiac remodeling rats. Further results also showed that the activation of PPARγ inhibited the expressions of Brg1 and TGF-β1 in the cardiac remodeling hearts. The activation of PPARγ also inhibited the proliferation and collagen production of cardiac fibroblasts, and down-regulated the activity of Brg1 and the expression of TGF-β1 induced by Ang II in cultured neonatal rat cardiomyocytes and cardiac fibroblasts, respectively, through NF-κB pathway. Conclusions: These results suggested that PPARγ activation effectively inhibited cardiac remodeling processes by suppression of Brg1 and TGF-β1 expressions through NF-κB pathway in the pressure-overloaded hearts induced by abdominal aorta ligation in rats. © 2015 S. Karger AG, Basel. Source

He J.,Harbin Medical University | Wang C.,Harbin Medical University | Sun Y.,First Hospital of Qiqihar | Lu B.,Harbin Medical University | And 5 more authors.
International Journal of Molecular Medicine

Exendin-4 (ex-4) is a long-acting glucagon-like peptide-1 receptor (GLP-1R) agonist which exerts beneficial effects on glycemic control and promotes cell viability. In the present study, we investigated the anti-apoptotic effects of ex-4, as well as the potential mechanisms responsible for these effects in rat bone marrow-derived mesenchymal stem cells (BM-MSCs) under conditions of oxygen, glucose and serum deprivation (OGD). The apoptosis of the MSCs was induced by subjecting the cells to OGD conditions for 4 h and was detected by Annexin V/PI and Hoechst 33258 staining. The MSCs were pre-conditioned with ex-4 for 12 h prior to being subjected to OGD conditions, and the expression levels of an apoptotic marker (cleaved caspase-3), endoplasmic reticulum (ER) stress markers [phosphorylated (p-)protein kinase RNA-like endoplasmic reticulum kinase (PERK), PERK, binding immunoglobulin protein (BIP), activating transcription factor 4 (ATF-4) and C/EBP homologous protein (CHOP)], as well as those of a survival marker (Bcl-2) were measured by western blot analysis. Furthermore, the mRNA levels of ATF-4 and CHOP were determined by RT-qPCR. ELISA was used to examine the activity of intracellular cAMP. Moreover, the GLP-1R antagonist, exendin9-39 (ex9-39), the protein kinase A (PKA) inhibitor, H89, and small interfering RNA (siRNA) targeting rat ATF-4 and CHOP were co-incubated with the MSCs. The apoptotic rate was markedly diminished following pre-conditioning with ex-4 in a dose-dependent manner (P<0.05). The ER stress markers, p-PERK, BIP, ATF-4 and CHOP, were upregulated in the cells subjected to OGD conditions. Ex-4 pre-conditioning significantly decreased the mRNA and protein levels of ATF-4 and CHOP (P<0.05), and increased the activity of intracellular cAMP (P<0.05). Furthermore, the anti-apoptotic effects of ex-4 were almost reversed by treatment with either H89 or ex9-39 (P<0.05); transfection with siRNA-CHOP significantly reduced the apoptotic rate of the MSCs and did not impair the cytoprotective effects of ex-4. Taken together, these findings suggest that ex-4 protects rat BM-MSCs from OGD-induced apoptosis through the activation of the PKA/cAMP pathway and the attenuation of the ER stress signaling pathway. Ex-4 may thus prove to be a therapeutic agent with the potential to improve the viability of MSCs in the ischemic milieu, and consequently, to optimize the therapeutic effects of MSC therapy in acute myocardial infarction. Source

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