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ROLE OF bcl-2 IN APOPTOSIS OF VASCULAR SMOOTH MUSCLE CELLS INDUCED BY NITRIC OXIDE
Author(s): 
Pages: 151-154
Year: Issue:  2
Journal: ACTA ANATOMICA SINICA

Keyword:  一氧化氮血管平滑肌细胞(VSMC)细胞凋亡bcl-2;
Abstract: Objective To explore the effect of bcl-2 in vascular smoot hmuscle cells(VSMC) apoptosi s induced by nitric oxide(NO),we investigated the effect of NO on Bcl -2 protein expression in cultured vascular smooth muscle cells(VSMCs),and effec t of Bcl-2 over expression on apoptosis is(VSMCs) induced by NO. Methods Cultured rat VSMCs at passage 5 to 8 were used for experiments,S-nitroso-N-acetypenicillamine(SNAP) was used as NO donor.Cells were preincubated for 24-48 hours in special culture dish with c onditioned medium to reach quiescent,and then incubated in conditioned medium co ntaining 0.5 mmol/L SNAP.After 8 to 10 hours,the cells were fixed and Bcl-2 ex p ression was analyzed by ACAS 570 through fluorescent immunochemistry.Vascular s mo oth muscle cells were transfected with bcl-2 gene through retrovirus to allow o verexpression of Bcl-2 in VSMCs.Finally,we observed the apoptosis in normal VSMCs and VSMCs infected with bcl-2. Results SNAP downregulated Bcl-2 expression in VSMCs.PCR and Southern hybridization confirmed the integration of the bcl-2 retrovirus vector into vascular smooth muscle cells genomic DNA.And fluorescenc e im munohistochemistry confirmed that Bcl-2 protein was overexpressed in VSMCs infected with bcl-2.And ratio of apoptosis become lower in VSMCs infected with bcl-2. Conclusion bcl-2 can inhibit apoptosis of VSMCs induced by SNAP.It is suggested that downregulation of Bcl-2 protein is o ne of the ways in which SNAP induces VSMCs apoptosis,and a pop tosis in VSMCs induced by SNAP is regulated by bcl-2.
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