A novel anti-inflammatory mechanism of high density lipoprotein through up-regulating annexin A1 in vascular endothelial cells
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- 作者：Bing Pana ; b ; c ; 1 ; Jinge Kongd ; e ; f ; g ; h ; 1 ; Jingru Jini ; k ; Jian Kongj ; Yubin Hek ; Shuying Dongj ; Liang Jia ; b ; c ; Donghui Liua ; b ; c ; Dan Hea ; b ; c ; Liming Kongl ; David K. Jinm ; Belinda Willardn ; Subramaniam Pennathuro ; Lemin Zhenga ; b ; c ; zhengl@bjmu.edu.cn" class="auth_mail" title="E-mail the corresponding author
- 关键词：HDL ; high-density lipoprotein ; CVD ; cardiovascular disease ; NO ; nitric oxide ; ROS ; reactive oxygen species ; TNF-α ; tumor necrosis factor α ; HUVECs ; human umbilical vein endothelial cells ; ANXA1 ; annexin A1 ; ANXA5 ; annexin A5 ; SR-BI ; scavenger receptor class B type I ; apo ; apolipoprotein ; TGF-β ; transforming growth factor β ; PKC ; protein kinase C ; MAPK ; mitogen-activated protein kinase ; ERK ; extracellular regulated protein kinases ; EMPs ; endothelium microparticles
- 刊名：Biochimica et Biophysica Acta (BBA)-Molecular and Cell Biology of Lipids
- 出版年：2016
- 出版时间：June 2016
- 年：2016
- 卷：1861
- 期：6
- 页码：501-512
- 全文大小：759 K
文摘
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HDL up-regulated endothelial annexin A1 via SR-BI and activation of ERK, p38MAPK, Akt and PKC signaling pathways.
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Endothelial ANXA 1 inhibited monocyte adhesion.
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High density lipoprotein-induced annexin A1 not only inhibited cell surface VCAM-1, ICAM-1, and E-selectin but also suppressed secretion of MCP-1, IL-8, VCAM-1 and E-selectin, which alleviated inflammatory response.