Hyper-activation of pp60^Src limits nitric oxide signaling by increasing asymmetric dimethylarginine levels during acute lung injury

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• 作者：Sanjiv Kumar^a ; Xutong Sun^b ; Satish Kumar Noonepalle^b ; Qing Lu^b ; Evgeny Zemskov^b ; Ting Wang^b ; Saurabh Aggarwal^c ; Christine Gross^a ; Shruti Sharma^d ; Ankit A Desai^b ; Yali Hou^a ; Sridevi Dasarathy^a ; Ning Qu^b ; Vijay Reddy^a ; Sung Gon Lee^a ; Mary Cherian-Shaw^a ; Jason X.-J. Yuan^b ; John D. Catravas^d ; Ruslan Rafikov^b ; Joe G.N. Garcia^b ; Stephen M. Black^b ; ^{steveblack@email.arizona.edu}
• 关键词：Signal transduction ; eNOS uncoupling ; Acute lung injury
• 刊名：Free Radical Biology and Medicine
• 出版年：2017
• 出版时间：January 2017
• 年：2017
• 卷：102
• 期：Complete
• 页码：217-228
• 全文大小：2195 K
• 卷排序：102

文摘

The disruption of the endothelial barrier by LPS involves the uncoupling of eNOS. LPS increases pp60Src activity, NO production, NOS uncoupling, and protein nitration. eNOS uncoupling correlated with a decrease in DDAH activity and an increase in ADMA. The decrease in DDAH activity was mediated by the phosphorylation of DDAH II at Y207.