MicroRNA-9 inhibits high glucose-induced proliferation, differentiation and collagen accumulation of cardiac fibroblasts by down-regulation of TGFBR2
| Autor: | Guoqian Wei, Jiaxin Li, Yingnan Dai, Zhendong Su |
|---|---|
| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
miRNA-9 Cardiac fibrosis Cell Survival Cellular differentiation cardiac fibrosis Biophysics Down-Regulation Biology Protein Serine-Threonine Kinases Transfection Biochemistry Transforming Growth Factor beta1 03 medical and health sciences Western blot Downregulation and upregulation medicine Humans Viability assay human cardiac fibroblasts Receptor Molecular Biology Cells Cultured Cell Proliferation Original Paper medicine.diagnostic_test Myocardium Receptor Transforming Growth Factor-beta Type II Cell Differentiation Cell Biology Fibroblasts medicine.disease Molecular biology Fibrosis Original Papers Up-Regulation high glucose TGFBR2 Blot MicroRNAs 030104 developmental biology Glucose Collagen Receptors Transforming Growth Factor beta Transforming growth factor |
| Zdroj: | Bioscience Reports |
| ISSN: | 1573-4935 |
| Popis: | To investigate the effects of miR-9 on high glucose (HG)-induced cardiac fibrosis in human cardiac fibroblasts (HCFs), and to establish the mechanism underlying these effects. HCFs were transfected with miR-9 inhibitor or mimic, and then treated with normal or HG. Cell viability and proliferation were detected by using the Cell Counting Kit-8 (CCK-8) assay and Brdu-ELISA assay. Cell differentiation and collagen accumulation of HCFs were detected by qRT-PCR and Western blot assays respectively. The mRNA and protein expressions of transforming growth factor-β receptor type II (TGFBR2) were determined by qRT-PCR and Western blotting. Up-regulation of miR-9 dramatically improved HG-induced increases in cell proliferation, differentiation and collagen accumulation of HCFs. Moreover, bioinformatics analysis predicted that the TGFBR2 was a potential target gene of miR-9. Luciferase reporter assay demonstrated that miR-9 could directly target TGFBR2. Inhibition of TGFBR2 had the similar effect as miR-9 overexpression. Down-regulation of TGFBR2 in HCFs transfected with miR-9 inhibitor partially reversed the protective effect of miR-9 overexpression on HG-induced cardiac fibrosis in HCFs. Up-regulation of miR-9 ameliorates HG-induced proliferation, differentiation and collagen accumulation of HCFs by down-regulation of TGFBR2. These results provide further evidence for protective effect of miR-9 overexpression on HG-induced cardiac fibrosis. |
| Databáze: | OpenAIRE |
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