RAGE signaling mediates post-injury arterial neointima formation by suppression of liver kinase B1 and AMPK activity.

Atherosclerosis
Weifang YuRobert Terkeltaub

Abstract

Intima formation involves smooth muscle cell (SMC) proliferation and migration that ultimately drives arterial stenosis, thrombosis, and ischemia in atherosclerosis, hypertension, and arterial revascularization. Receptor for advanced glycation endproducts (RAGE) is a transmembrane signaling receptor implicated in diabetic renal and vascular complications, and post-injury intima formation, partly via Signal transducer and activator of transcription 3 (STAT3) activation. The metabolic super-regulator Adenosine monophosphate kinase (AMPK) inhibits SMC proliferation and intima formation. AMPK activation is promoted by liver kinase B1 (LKB1), and LKB1 inhibits STAT3 activation. Here, we tested the hypothesis that RAGE promotes arterial intima formation by modulating both LKB1 and AMPK. RAGE ligands (the calgranulin S100A11, and glycated albumin) suppressed AMPK activation in conjunction with increased proliferation and migration of cultured SMCs. These effects were inhibited both by RAGE deficiency and by prior AMPK activation. In SMCs, RAGE ligands decreased LKB1 activity. Moreover, knockdown of both LKB1 and AMPK were associated with increased STAT3 phosphorylation levels. In response to murine carotid artery ligation, expression ...Continue Reading

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Citations

Nov 15, 2013·Biomedical Journal·Walter Gottlieb Land
Apr 2, 2013·Journal of Leukocyte Biology·Katrin Kierdorf, Günter Fritz
Dec 11, 2019·Journal of Cellular and Molecular Medicine·Shiu-Wen HuangMing-Jen Hsu
Jun 29, 2021·Frontiers in Cell and Developmental Biology·Linqiang ZhangBin Liang

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