Glucose-induced endothelin-1 expression is regulated by ERK5 in the endothelial cells and retina of diabetic rats

Canadian Journal of Physiology and Pharmacology
Yuexiu WuSubrata Chakrabarti

Abstract

Upregulation of endothelin 1 (ET-1) causing blood flow alteration and increased extracellular matrix production are characteristic features of diabetic angiopathy. Several glucose-induced signaling mechanisms cause ET-1 upregulation in diabetic angiopathy. Extracellular signal-regulated kinase 5 (ERK5) is a member of the MAPK family, which plays a key role in cardiovascular development. ERK kinase (MEK) 5 is the specific MEK for ERK5 activation. In this study we examined the role of glucose-induced ERK5 signaling in mediating ET-1 expression in diabetic angiopathy. We investigated retinas from 1-month STZ-induced diabetic rats and human macro- and microvascular endothelial cells to study ERK5-dependent ET-1 alterations. Glucose (25 mmol/L) caused significant upregulation of ET-1 mRNA and downregulation of ERK5 and Kruppel-like factor 2 (KLF2) after 24 h treatment in the endothelial cells. Simultaneously, phospho-ERK5 proteins were reduced. Activation of ERK5 by constitutively active MEK5 (caMEK5) upregulated KLF2 and suppressed ET-1 expression in both cell lines, whereas ERK5 siRNA transfection resulted in decreased ERK5 and KLF2 and increased ET-1 mRNA expression. In addition, caMEK5 prevented glucose-induced upregulation of E...Continue Reading

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Citations

Dec 23, 2011·Basic Research in Cardiology·Hanrui ZhangCuihua Zhang
May 30, 2013·Indian Journal of Dermatology·Xinhong GeJianzhong Zhang
May 13, 2015·Seminars in Nephrology·Elena GagliardiniAriela Benigni
Jun 28, 2018·Physiological Research·W LiA Ergul
Jan 11, 2020·Frontiers in Endocrinology·Saumik BiswasSubrata Chakrabarti
Mar 11, 2015·Journal of Cellular and Molecular Medicine·Rokhsana MortuzaSubrata Chakrabarti

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