Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 391, Issue 1, Pages 85-90Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2009.11.008
Keywords
Angiotensin II receptors; Signal cross-talk; Dimerization; Inositol phosphate production; Phospholipase C
Categories
Funding
- Ministry of Education, Culture, Sports, Science and Technology, Japan [18590916, 21591065]
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL057470] Funding Source: NIH RePORTER
Ask authors/readers for more resources
Although angiotensin II (Ang II) binds to Ang II type I (AT(1)) and type 2 (AT(2)) receptors. AT(1) and AT(2) receptors have antagonistic actions with regard to cell signaling. The molecular mechanisms that underlie this antagonism are not well understood. We examined AT(1) and AT(2) receptor-induced signal cross-talk in the cytoplasm and the importance of the hetero-dimerization of AT(1) receptor with AT(2) receptor on the cell surface. AT(1) and AT(2) receptors showed antagonistic effects toward inositol phosphate production AT(1) receptors mainly formed homo-dimers, rather than hetero-dimers with AT(2) receptor, on the cell surface as determined by immunoprecipitation, and subsequently induced cell signals AT(2) receptor mainly formed homo-dimers. rather than hetero-dimers with AT(1) receptor, on the cell surface. The expression levels of homo-dimerized AT(1) receptor or AT(2) receptor on the cell surface did not change after treatment with Ang II, the AT(1) receptor antagonist telmisartan or the AT(2) receptor antagonist PD123319 Finally, AT(1) and AT(2) receptor-induced signals antagonized phospholipase C-beta(3) phosphorylation in conclusion, Ang II-induced AT(1) receptor signals may be mainly blocked by AT(2) receptor signals through their negative cross-talk in the cytoplasm rather than by the hetero-dimerization of both receptors on the cell surface. The proper balance of the expression levels of AT(1) and AT(2) receptors might be critical for the antagonistic action between these receptors. (C) 2009 Elsevier Inc All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available