Angiotensin II Stimulation of NADPH oxidase Activity and Secretion of Cyclophilin-A in Adventitial Fibroblasts; Potential Role in the Paracrine Mediation of Vascular Smooth Muscle Cell Hypertrophy
Loading...
Authors
Iqbal, Tania R.
Issue Date
2005
Type
Thesis
Language
en_US
Keywords
Alternative Title
Abstract
Superoxide (02) derived from NADPH oxidase is thought to contribute to the cause of
hypertension. O2 is found at elevated levels in many disease states such as atherosclerosis, diabetes, and restenosis. It has been reported that angiotensin II (AngII) stimulates NADPH oxidase-derived reactive oxygen species in the adventitia and intima concomitant with medial hypertrophy (Rey et al., 2002). We hypothesized that increasing the activity of NADPH oxidase in adventitial fibroblasts with angiotensin II causes the release of hormones that increase hypertrophy of the media, and that these factors increase hypertrophy by activating the ERKI/2 pathway. To better understand how the adventitia might affect medial hypertrophy, fibroblasts, the major cell type in the adventitia, were studied. Using an NADPH oxidase activity assay, a proliferation assay, and Western blotting, we determined that the proliferation of fibroblasts and secretion of cyclophilin-a in response to AngII were NADPH oxidase dependent.
Description
v, 36 p.
Citation
Publisher
Kalamazoo College
License
U.S. copyright laws protect this material. Commercial use or distribution of this material is not permitted without prior written permission of the copyright holder.