Metallothionein rescues hypoxia-inducible factor-1 transcriptional activity in cardiomyocytes under diabetic conditions

18Citations
Citations of this article
18Readers
Mendeley users who have this article in their library.
Get full text

Abstract

Metallothionein (MT) is effective in the prevention of diabetic cardiomyopathy, and hypoxia-inducible factor-1 (HIF-1) is known to control vascular endothelial growth factor (VEGF) gene expression and regulate angiogenesis in diabetic hearts. We examined whether or not MT affects HIF-1 activity in the heart of diabetic mice and in the cardiac cells cultured in high glucose (HG) media. Diabetes was induced by streptozotocin in a cardiac-specific MT overexpressing transgenic mouse model. The primary cultures of neonatal cardiomyocytes and the embryonic rat cardiac H9c2 cell line were cultured in HG media. HIF-1 and VEGF were determined by immunofluorescent staining and enzyme-linked immunosorbent assay, respectively. The H9c2 cells were transfected with a hypoxia-responsive element-dependent reporter plasmid and the HIF-1 transcriptional activity was measured by luciferase reporter assay. MT overexpression increased HIF-1α in diabetic hearts. HG suppressed CoCl2-induced VEGF expression in primary cultures of neonatal cardiomyocytes and MT overexpression suppressed the inhibition. The addition of MT into the cultures of H9c2 cells relieved the HG suppression of hypoxia-induced luciferase activity. This study indicates that MT can rescue HIF-1 transcriptional activity in cardiomyocytes under diabetic conditions. © 2007 Elsevier Inc. All rights reserved.

Cite

CITATION STYLE

APA

Feng, W., Wang, Y., Cai, L., & Kang, Y. J. (2007). Metallothionein rescues hypoxia-inducible factor-1 transcriptional activity in cardiomyocytes under diabetic conditions. Biochemical and Biophysical Research Communications, 360(1), 286–289. https://doi.org/10.1016/j.bbrc.2007.06.057

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free