ROS-activated calcium signaling mechanisms regulating endothelial barrier function
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- 作者：Anke Di ; Dolly Mehta ; Asrar B. Malik ; abmalik@uic.edu" class="auth_mail" title="E-mail the corresponding author
- 关键词：AJs ; adherence junctions ; ALI ; acute lung injury ; ARDS ; acute respiratory distress syndrome ; Cav-1 ; caveolin-1 ; CRAC ; calcium-release-activated calcium channel ; CSD ; cav-1 scaffold domain ; DAG ; diacylglycerol ; EC ; endothelial cells ; ER ; endoplasmic reticulum ; ERM ; ezrin-radixin-moesin ; GDI ; GDP dissociation inhibitor ; GDP ; guanosine diphosphate ; HEK293T ; XXX ; ICAM-1 ; intercellular adhesion molecule 1 ; IP3R3 ; inositol 1 ; 4 ; 5-trisphosphate receptor 3 ; LPS ; lipopolysaccharide ; MLC ; myosin light chai
- 刊名：Cell Calcium
- 出版年：2016
- 出版时间：September 2016
- 年：2016
- 卷：60
- 期：3
- 页码：163-171
- 全文大小：1850 K
文摘
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Increased reactive oxygen species (ROS) generated in tissue during inflammation play an important role in the development of ALI and its progression to ARDS.
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ROS initiated Ca2+ signaling in tissue plays an important role in increasing endothelial permeability.
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Redox sensitive TRPM2 channel and TRPC6 and other TRPCs such as TRPC1 which form CRAC by connecting with ORAI and ROS sensor STIM1, are key players in mediating ROS-induced Ca2+ signaling in regulating endothelial permeability upon oxidant stress.