Homocysteine directly interacts and activates the angiotensin II type I receptor to aggravate vascular injury View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2018-12

AUTHORS

Tuoyi Li, Bing Yu, Zhixin Liu, Jingyuan Li, Mingliang Ma, Yingbao Wang, Mingjiang Zhu, Huiyong Yin, Xiaofeng Wang, Yi Fu, Fang Yu, Xian Wang, Xiaohong Fang, Jinpeng Sun, Wei Kong

ABSTRACT

Hyperhomocysteinemia (HHcy) is a risk factor for various cardiovascular diseases. However, the mechanism underlying HHcy-aggravated vascular injury remains unclear. Here we show that the aggravation of abdominal aortic aneurysm by HHcy is abolished in mice with genetic deletion of the angiotensin II type 1 (AT1) receptor and in mice treated with an AT1 blocker. We find that homocysteine directly activates AT1 receptor signalling. Homocysteine displaces angiotensin II and limits its binding to AT1 receptor. Bioluminescence resonance energy transfer analysis reveals distinct conformational changes of AT1 receptor upon binding to angiotensin II and homocysteine. Molecular dynamics and site-directed mutagenesis experiments suggest that homocysteine regulates the conformation of the AT1 receptor both orthosterically and allosterically by forming a salt bridge and a disulfide bond with its Arg167 and Cys289 residues, respectively. Together, these findings suggest that strategies aimed at blocking the AT1 receptor may mitigate HHcy-associated aneurysmal vascular injuries. More... »

PAGES

11

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/s41467-017-02401-7

DOI

http://dx.doi.org/10.1038/s41467-017-02401-7

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1100092807

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/29296021


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