The renin-angiotensin system is upregulated in pregnant women and may play a role in myometrial hypertrophy during pregnancy. We examined whether angiotensin II could induce myometrial protein synthesis as determined by 3H-leucine incorporation in an immortalized human myometrial smooth muscle cell line (ULTR cells). The effects of angiotensin II were mediated by NADPH oxidase because diphenylene iodonium abolished angiotensin II-induced protein synthesis. We investigated gene expression and cellular localization of NADPH oxidase isoforms in ULTR cells and confirmed expression of NOX1, NOX4, and NOX5 in myometrial tissue. Angiotensin II induced a cellular redistribution and upregulation of NOX5 protein without altering NOX1 and NOX4 expression. It seems the effect of angiotensin II relies on the type 1 receptor (AT1), because losartan significantly blocked angiotensin II-induced increase in 3H-leucine incorporation. We conclude that NADPH oxidase mediates angiotensin II-stimulated protein synthesis downstream of AT1 in myometrium smooth muscle cells.
You have requested a machine translation of selected content from our databases. This functionality is provided solely for your convenience and is in no way intended to replace human translation. Neither BioOne nor the owners and publishers of the content make, and they explicitly disclaim, any express or implied representations or warranties of any kind, including, without limitation, representations and warranties as to the functionality of the translation feature or the accuracy or completeness of the translations.
Translations are not retained in our system. Your use of this feature and the translations is subject to all use restrictions contained in the Terms and Conditions of Use of the BioOne website.
Vol. 82 • No. 2