An involvement of SR-B1 mediated PI3K-Akt-eNOS signaling in HDL-induced cyclooxygenase 2 expression and prostacyclin production in endothelial cells

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• 作者：Qing-Hai Zhang^a ; ^b ; Xu-Yu Zu^a ; Ren-Xian Cao^a ; Jiang-Hua Liu^a ; Zhong-Cheng Mo^b ; Ying Zeng^b ; Yuan-Bin Li^b ; Sheng-Lin Xiong^b ; Xing Liu^b ; Duan-Fang Liao^c ; Guang-Hui Yi^b ; ^{ghyi6108@163.com}
• 关键词：HDL ; high-density lipoprotein ; apoA1 ; apolipoprotein A-1 ; SR-B1 ; scavenger receptor class B type 1 ; eNOS ; endothelial nitric oxide synthase ; p38MAPK ; p38 mitogen activated protein kinase ; CREB ; cAMP-response element binding protein ; PGIS ; prostacyclin syn
• 刊名：Biochemical and Biophysical Research Communications
• 出版年：2012
• 期刊代码：159_0006291x
• 类别：bio
• 出版时间：30 March, 2012
• 卷：420
• 期：1
• 页码：17-23
• 文件大小：773 K

摘要

It is well-known that sphingosine-1-phosphate (S1P), the phospholipid content of HDL, binding to S1P receptors can raise COX-2 expression and PGIb>2b> release through p38MAPK/CREB pathway. In the present study we assess the action of SR-B1 initiated PI3K-Akt-eNOS signaling in the regulation of COX-2 expression and PGIb>2b> production in response to HDL. We found that apoA1 could increase PGIb>2b> release and COX-2 expression in ECV 304 endothelial cells. Furthermore, SR-B1 was found to be involved in HDL induced up-regulation of COX-2 and PGIb>2b>. Over-expressed SR-B1 did not significantly increase the expression of COX-2 and the PGIb>2b> levels, but knock-down of SR-B1 by siRNA could significantly attenuate COX-2 expression and PGIb>2b> release together with p38MAPK and CREB phosphorylation. Consistently, the declines of p-p38MAPK, p-CREB, COX-2 and PGIb>2b> were also observed after incubation with LY294002 (25 渭mol/L; PI3K special inhibitor) or L-NAME (50 渭mol/L; eNOS special inhibitor). In addition, we demonstrated the increases of PGIb>2b> release, COX-2 expression and p38MAPK phosphorylation, when nitric oxide level was raised through the incubation of L-arginine (10 or 20 nmol/L) in endothelial cells. Taking together, our data support that SR-B1 mediated PI3K-Akt-eNOS signaling was involved in HDL-induced COX-2 expression and PGIb>2b> release in endothelial cells.