Open AccessAquaporin 1, Nox1, and Ask1 mediate oxidant-induced smooth muscle cell hypertrophy
Author(s) -
Imad Al Ghouleh,
Giovanna Frazziano,
Andrés Rodríguez,
Gábor Csányi,
Salony Maniar,
Claudette M. St. Croix,
Eric E. Kelley,
Loreto Egaña,
Gyun Jee Song,
Alessandro Bisello,
Yong J. Lee,
Patrick J. Pagano
Publication year - 2012
Publication title -
cardiovascular research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.774
H-Index - 219
eISSN - 1755-3245
pISSN - 0008-6363
DOI - 10.1093/cvr/cvs295
Subject(s) - nox1 , nadph oxidase , reactive oxygen species , microbiology and biotechnology , superoxide , vascular smooth muscle , chemistry , muscle hypertrophy , medicine , endocrinology , biology , biochemistry , enzyme , smooth muscle
Reactive oxygen species (ROS)-mediated intracellular signalling is well described in the vasculature, yet the precise roles of ROS in paracrine signalling are not known. Studies implicate interstitial ROS hydrogen peroxide (H(2)O(2)) in vascular disease, and plasma H(2)O(2) levels in the micromolar range are detectable in animal models and humans with hypertension. Recently, H(2)O(2) was shown to cross biological membranes of non-vascular cells via aquaporin (Aqp) water channels. Previous findings suggest that H(2)O(2) activates NADPH oxidase (Nox) enzymes in vascular cells and apoptosis signal-regulating kinase 1 (Ask1) in non-vascular cells. We hypothesized that extracellular H(2)O(2) induces smooth muscle cell (SMC) hypertrophy by a mechanism involving Aqp1, Nox1, and Ask1.
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