Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P10415 (Bcl-2)
 33,771 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Migration, proliferation and apoptosis of vascular smooth muscle cells (VSMCs) have recently been identified as important processes in a variety of human vascular diseases, including atherosclerosis, arterial injury, and restenosis after angioplasty. These processes are regulated by interactions between the local cell-cell and cytokine environment. Cytokine induced apoptosis inhibitor (CIAPIN1) is a novel antiapoptotic molecule and plays a vitally important role in malignant phenotypes of cancers. However, the effect of CIAPIN1 on VSMCs has not been reported. In the present study, we constructed the adenovirus encoding CIAPIN1 siRNA and transduced it into VSMCs. The results demonstrated that CIAPIN1 siRNA inhibited proliferation, migration and promotes apoptosis of VSMCs by regulating Bcl-2 and Bax. Our results suggest that CIAPIN1 siRNA might play the key role in VSMC biological function and provide the new therapeutic strategy for vascular diseases.
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PMID:CIAPIN1 siRNA inhibits proliferation, migration and promotes apoptosis of VSMCs by regulating Bcl-2 and Bax. 2315 Oct 78

Myocardial infarction (MI), a type of ischemic heart disease, is generally accompanied by apoptosis of cardiomyocytes. MicroRNAs play the vital roles in the development and physiology of MI. Here, we established a downregulation model of miR-182-5p in H9c2 cells under hypoxic conditions to investigate the potential molecular mechanisms for miR-182-5p in hypoxia-induced cardiomyocyte apoptosis (HICA). RT-qPCR indicated that miR-182-5p levels exhibit a time-dependent increase in the rate of apoptosis induced by hypoxia. The results from the MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) and LDH (lactate dehydrogenase) assays indicated that cardiomyocyte injury noticeably increased after exposure to hypoxia. Meanwhile, hypoxia dramatically increased the apoptosis rate [which was reflected in the results from the annexin V - propidium iodide (PI) assay], enhanced caspase-3 activity, and reduced the expression of Bcl-2. Downregulation of miR-182-5p can significantly reverse hypoxia-induced cardiomyocyte injury or apoptosis. Importantly, bioinformatic analysis and dual-luciferase reporter assay revealed that CIAPIN1 (cytokine-induced apoptosis inhibitor 1) was a direct functional target of miR-182-5p, and that inhibition of miR-182-5p can lead to an increase in CIAPIN1 expression at both the mRNA and protein levels. Furthermore, the knockdown of CIAPIN1 with small interfering RNAs (siRNAs) efficiently abolished the protective effects of miR-182-5p inhibitor on HICA, demonstrating that miR-182-5p plays a pro-apoptotic role in cardiomyocytes under hypoxic conditions by downregulating CIAPIN1. Collectively, our results demonstrate that miR-182-5p may serve an underlying target to prevent cardiomyocytes from hypoxia-induced injury or apoptosis.
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PMID:Inhibition of miR-182-5p protects cardiomyocytes from hypoxia-induced apoptosis by targeting CIAPIN1. 2967 38