Activation of vascular p38MAPK by mechanical stretch is independent of c-Src and NADPH oxidase: Influence of hypertension and angiotensin II

Paravicini, Tamara M., Montezano, Augusto C., Yusuf, Hiba and Touyz, Rhian M. (2012) Activation of vascular p38MAPK by mechanical stretch is independent of c-Src and NADPH oxidase: Influence of hypertension and angiotensin II. Journal of the American Society of Hypertension, 6 3: 169-178.


Author Paravicini, Tamara M.
Montezano, Augusto C.
Yusuf, Hiba
Touyz, Rhian M.
Title Activation of vascular p38MAPK by mechanical stretch is independent of c-Src and NADPH oxidase: Influence of hypertension and angiotensin II
Journal name Journal of the American Society of Hypertension  (ERA 2012 Listed)   Check publisher's open access policy
Publication date 2012-05
Sub-type Article
DOI 10.1016/j.jash.2012.01.002
Volume number 6
Issue number 3
ISSN 1878-7436; 1933-1711
Start page 169
End page 178
Total pages 10
Place of publication Philadelphia, PA, United States
Publisher Elsevier
Collection year 2013
Language eng
Formatted abstract Little is known about vascular MAPK regulation in response to mechanical strain. Whether mechanically-sensitive pathways are altered in hypertension is unclear. We examined effects of stretch and Ang II on activation of p38MAPK in vascular smooth muscle cells (VSMC) from WKY and SHR. The role of c-Src and redox-sensitive pathways in stretch-induced effects were examined. VSMC from mesenteric arteries were plated onto flexible silastic plates and exposed to acute or chronic cyclic stretch (10%, 1 Hz) with or without Ang II (0.1 uM). Acute stretch stimulated p38MAPK activation in WKY and SHR, independently of c-Src and reactive oxygen species (ROS), since PP2 (c-Src inhibitor) and apocynin (NADPH oxidase inhibitor), failed to alter stretch-mediated p38MAPK. Chronic stretch blunted p38MAPK phosphorylation in WKY and increased phosphorylation in SHR. Stretch, in the presence of Ang II, induced an increase in procollagen-1 expression. This was blocked by SB203580 (p38MAPK inhibitor). Accordingly, vascular p38MAPK is a mechano-sensitive MAPK, differentially regulated by acute and chronic stretch in WKY and SHR. Functionally, stretch and Ang II, amplify profibrotic responses in a p38MAPK-dependent manner, responses that are perturbed in SHR. Such molecular process may influence vascular fibrosis in hypertension and appear to be independent of c-Src and ROS.
Keyword Mechanical strain
Vascular remodeling
MAP kinases
SHR
Signal transduction
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article
Collections: Official 2013 Collection
School of Biomedical Sciences Publications
 
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