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　　报告题目：Endothelial dysfunction: Regenerate to be old

　　报告人：Paul M. Vanhoutte, M.D., Ph.D.，Chair Professor

　　State Key Laboratory of Pharmaceutical Biotechnology and Department of Pharmacology and Pharmacy, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong, China

　　时间：2015年4月21日上午10:00

　　地点：生化楼三楼中厅

　　主持人：杨宝学教授

　　报告内容简介

　　The endothelium mediates endothelium-dependent relaxations of the underlying vascular smooth muscle cells by releasing endothelium-derived relaxing factors (EDRF). The best characterized EDRF is nitric oxide (NO). The release of NO can be mediated by both pertussis toxin-sensitive Gi-and insensitive Gq-proteins. The ability of the endothelial cell to release relaxing factors can be up-regulated by estrogens, exercise and antioxidants, and down-regulated by oxidative stress and increased presence of oxidized LDL. Following injury or apoptotic death, the endothelium regenerates, resulting in an early selective loss of the pertussis-toxin sensitive mechanisms of EDRF-release. Functional studies suggest that increased presence of oxidized LDL (due to oxidative stress) plays a key role in this selective loss. Genomic studies demonstrate the emergence of fatty acid binding protein-A (A-FBP) and metalloproteinase-7 (MMP7) in regenerated endothelial cells. Inhibition of A-FABP curtails the occurrence of endothelial dysfunction.  The reduced release of NO resulting from the endothelial dysfunction in regenerated areas sets the stage for the occurrence of vasospasm and thrombosis as well as it permits the inflammatory response leading to atherosclerosis.

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