Institute of Pharmacy and Pharmacology

Hengyang, China

Institute of Pharmacy and Pharmacology

Hengyang, China
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Yang X.,Institute of Biologic Research | Yang X.,Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study | Yin J.,Institute of Biologic Research | Xiang Q.,Institute of Pharmacy and Pharmacology | And 6 more authors.
Journal of Central South University (Medical Sciences) | Year: 2017

Objective: To investigate effects of miR-503 on cisplatin sensitivity in BEL-7402 cells by targeting ofbcl-2. Methods: MiR-503 and bcl-2 mRNA expression levels in hepatocellular carcinoma cells were measured by real-time quantitative (qRT)-PCR; Bel-protein level was detected by Western blot; miR-503 mimics were transiently transfected to the BEL-7402 cells by liposome transfection; potential target genes of miR-503 were predicted by Bioinformatics software; miR-503 potential targets were validated by dual luciferase activity; and the cell viability was measured by MTT assay. Results: MiR-503 level was down-regulated and Bcl-2 protein expression level was up-regulated in BEL-7402 cells compared with HL-7702 cells. MiR-503 could interact with bcl-2 and inhibit its expression. Cell vitality with miR-503 transfection was significantly reduced compared to that in the negative control. Conclusion: MiR-503 may enhance the sensitivity of BEL-7402 cells to cisplatin and inhibit the cell proliferation by targeting bcl-2.


Luo D.-x.,Institute of Pharmacy and Pharmacology | Luo D.-x.,Central South University | Luo D.-x.,The First Peoples Hospital of Chenzhou City | Cheng J.,University of Illinois at Springfield | And 9 more authors.
Biochemical and Biophysical Research Communications | Year: 2010

Intimal hyperplasia plays an important role in various types of vascular remodeling. Mechanical forces derived from blood flow are associated with the proliferation of vascular smooth muscle cells (VSMC). This contributes to many vascular disorders such as hypertension, atherosclerosis and restenosis after percutaneous transluminal angioplasty (PTA). In this study, we show that static pressure induces the proliferation of VSMC and activates its related signal pathway. VSMC from a rat aorta were treated with different pressures (0, 60, 90, 120, 150 and 180 mm Hg) in a custom-made pressure incubator for 24 h. The most active proliferation of VSMC was detected at a pressure of 120 mm Hg. VSMC was also incubated under a static pressure of 120 mm Hg for different time intervals (0, 2, 4, 8, 12 and 24 h). We found that static pressure significantly stimulates VSMC proliferation. Extracellular signal-regulated kinases 1/2 (ERK1/2) activation showed a peak at the pressure of 120 mm Hg at 4-h time point. Moreover, caveolin-1 expression was significantly inhibited by rising static pressure. Downregulation of VSMC proliferation could be found after PD98059 (ERK1/2 phosphorylation inhibitor) treatment. Our data also showed that a siRNA-mediated caveolin-1 knock down increased ERK1/2 phosphorylation and VSMC proliferation. These results demonstrate that static pressure promotes VSMC proliferation via the Caveolin-1/ERK1/2 pathway. © 2009 Elsevier Inc. All rights reserved.

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