KMID : 0311120160570010247
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Yonsei Medical Journal 2016 Volume.57 No. 1 p.247 ~ p.253
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Galpha12 Protects Vascular Endothelial Cells from Serum Withdrawal-Induced Apoptosis through Regulation of miR-155
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Lee Hyeon-Jeong
Lee Eun-Jig Seo Mi-Ran
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Abstract
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Purpose : Apoptosis of vascular endothelial cells is a type of endothelial damage that is associated with the pathogenesis of cardiovascular diseases such as atherosclerosis. Heterotrimeric GTP-binding proteins (G proteins), including the alpha 12 subunit of G protein (G¥á12), have been found to modulate cellular proliferation, differentiation, and apoptosis of numerous cell types. However, the role of G¥á12 in the regulation of apoptosis of vascular cells has not been elucidated. We investigated the role of G¥á12 in serum withdrawal-induced apoptosis of human umbilical vein endothelial cells (HUVECs) and its underlying mechanisms.
Materials and Methods : HUVECs were transfected with G¥á12 small-interfering RNA (siRNA) to knockdown the endogenous G¥á12 expression and were serum-deprived for 6 h to induce apoptosis. The apoptosis of HUVECs were assessed by Western blotting and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. The expressions of microRNAs were analyzed by quantitative real-time PCR.
Results : Knockdown of G¥á12 with siRNA augmented the serum withdrawal-induced apoptosis of HUVECs and markedly repressed the expression of microRNA-155 (miR-155). Serum withdrawal-induced apoptosis of HUVECs was inhibited by the overexpression of miR-155 and increased significantly due to the inhibition of miR-155. Notably, the elevation of miR-155 expression prevented increased apoptosis of G¥á12-deficient HUVECs.
Conclusion : From these results, we conclude that G¥á12 protects HUVECs from serum withdrawal-induced apoptosis by retaining miR-155 expression. This suggests that G¥á12 might play a protective role in vascular endothelial cells by regulating the expression of microRNAs.
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KEYWORD
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G¥á12 protein, apoptosis, microRNAs, endothelial cells
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