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연세대학교 의과대학 Yonsei Medical Journal Yonsei Medical Journal 제57권 제1호
발행연도
2016.1
수록면
247 - 253 (7page)

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Purpose: Apoptosis of vascular endothelial cells is a type of endothelial damage that is associated with the pathogenesis of cardiovasculardiseases such as atherosclerosis. Heterotrimeric GTP-binding proteins (G proteins), including the alpha 12 subunit ofG protein (Gα12), have been found to modulate cellular proliferation, differentiation, and apoptosis of numerous cell types. However,the role of Gα12 in the regulation of apoptosis of vascular cells has not been elucidated. We investigated the role of Gα12 inserum withdrawal-induced apoptosis of human umbilical vein endothelial cells (HUVECs) and its underlying mechanisms. Materials and Methods: HUVECs were transfected with Gα12 small-interfering RNA (siRNA) to knockdown the endogenousGα12 expression and were serum-deprived for 6 h to induce apoptosis. The apoptosis of HUVECs were assessed by Western blottingand terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. The expressions of microRNAs were analyzedby quantitative real-time PCR. Results: Knockdown of Gα12 with siRNA augmented the serum withdrawal-induced apoptosis of HUVECs and markedly repressedthe expression of microRNA-155 (miR-155). Serum withdrawal-induced apoptosis of HUVECs was inhibited by the overexpressionof miR-155 and increased significantly due to the inhibition of miR-155. Notably, the elevation of miR-155 expressionprevented increased apoptosis of Gα12-deficient HUVECs. Conclusion: From these results, we conclude that Gα12 protects HUVECs from serum withdrawal-induced apoptosis by retainingmiR-155 expression. This suggests that Gα12 might play a protective role in vascular endothelial cells by regulating the expressionof microRNAs.

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