Ammonia promotes endothelial cell survival via the heme oxygenase-1-mediated release of carbon monoxide

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• 作者：Xiao-Ming Liu ; Kelly J. Peyton ; William Durante ; ^{durantew@health.missouri.edu}
• 关键词：HO-1 ; heme oxygenase-1 ; Nrf2 ; NF-E2-related factor-2 ; ROS ; reactive oxygen species ; CO ; carbon monoxide ; HUVECs ; human umbilical vein endothelial cells ; MAECs ; mouse aortic endothelial cells ; MASMCs ; mouse aortic smooth muscle cells ; NH4Cl ; ammonium chloride ; NH4OH ; ammonium hydroxide ; NAC ; N-acetyl-L-cysteine ; PMSF ; phenylmethylsulfonyl fluoride ; CM-H2DCFDA ; 5-(and-6)-chloromethyl-2 ; 7-dichlorodihydrofluorescein diacetate acetyl ester ; GSK3β ; glycogen synthase kinase-3β ; GSK3β-P ; phospho (ser-9)
• 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：37-46
• 全文大小：724 K
• 卷排序：102

文摘

Ammonia stimulates HO-1 expression in endothelial cells via the ROS-Nrf2 pathway. Glutamine induces HO-1 expression in endothelial cells via the formation of ammonia. Ammonia enhances endothelial cell viability via the HO-1-mediated release of CO. Ammonia is an important signaling gas that promotes endothelial cell survival.