Aminoguanidine normalizes ET-1-induced aortic contraction in type 2 diabetic Otsuka Long-Evans Tokushima Fatty (OLETF) rats by suppressing Jab1-mediated increase in ETA-receptor expression

Article ID	Journal	Published Year	Pages	File Type
10835888	Peptides	2012	11 Pages	PDF

Abstract

âº In type 2 diabetes, AG normalizes ET-1-induced aortic contraction by suppressing ETA-R/ERK activities through normalization of the imbalance between Jab1-modified ETA-R and O-GlcNAcylated ETA-R.

Keywords

HDL von Hippel–Lindau tumor suppressor protein Jab1 Otsuka Long–Evans Tokushima Fatty rat endothelin type B receptor O-GlcNAc ECE1 HIF1α IRS1 receptor for AGEs pVHL NEFA RAGE ERK CML ET-1 AGEs GPCRs G protein-coupled receptors MAPK Aminoguanidine Endothelin converting enzyme Non-esterified fatty acid endothelin-1 Diabetes insulin receptor substrate 1 LETO hypoxia-inducible factor 1 alpha high-density lipoprotein cholesterol LDL advanced glycation end-products OLETF rat mitogen-activated protein kinase Low-density lipoprotein cholesterol extracellular signal-regulated kinase endothelin type A receptor

Related Topics

Life Sciences Biochemistry, Genetics and Molecular Biology Biochemistry

Aminoguanidine normalizes ET-1-induced aortic contraction in type 2 diabetic Otsuka Long-Evans Tokushima Fatty (OLETF) rats by suppressing Jab1-mediated increase in ETA-receptor expression

Authors

Shingo Nemoto, Kumiko Taguchi, Takayuki Matsumoto, Katsuo Kamata, Tsuneo Kobayashi,