Activation of spleen tyrosine kinase is required for TNF-伪-induced endothelin-1 upregulation in human aortic endothelial cells

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• 作者：Yoon Ji Kim^a ; Tai Yeon Koo^a ; Won Seok Yang^a ; Nam Jeong Han^b ; Jin Uk Jeong^a ; Sang Koo Lee^a ; Su-Kil Park^a ; ^{skpark@amc.seoul.kr}
• 关键词：Activator protein-1 ; Endothelin-1 ; Reactive oxygen species ; Spleen tyrosine kinase ; Tumor necrosis factor-伪
• 刊名：FEBS Letters
• 出版年：2012
• 期刊代码：70_00145793
• 类别：bio
• 出版时间：23 March, 2012
• 卷：586
• 期：6
• 页码：818-826
• 文件大小：998 K

摘要

Endothelin-1 (ET-1) promotes atherosclerosis. We tested whether spleen tyrosine kinase (Syk) mediates tumor necrosis factor-伪 (TNF-伪)-induced ET-1 upregulation in human aortic endothelial cells (HAECs) and sought to identify the signal pathways involved. TNF-伪-induced reactive oxygen species (ROS) activated Syk and phosphatidylinositol 3-kinase (PI3K), which was required for the activation of AP-1 and subsequent ET-1 gene transcription. ROS mediated c-Jun NH₂-terminal kinase (JNK) is also required for AP-1 activation, but Syk and PI3K regulated AP-1 activation independently of JNK. Through regulation of ET-1 production, Syk could be implicated in atherosclerosis.