MEF2B-Nox1 Signaling Is Critical for Stretch-Induced Phenotypic Modulation of Vascular Smooth Muscle Cells | Zendy

Andrés Rodríguez | Zendy; Gábor Csányi | Zendy; Daniel J. Ranayhossaini | Zendy; Douglas M. Feck | Zendy; Kory J. Blose | Zendy; Lillian Assatourian | Zendy; David A. Vorp | Zendy; Patrick J. Pagano | Zendy

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MEF2B-Nox1 Signaling Is Critical for Stretch-Induced Phenotypic Modulation of Vascular Smooth Muscle Cells

Author(s) -

Andrés Rodríguez,

Gábor Csányi,

Daniel J. Ranayhossaini,

Douglas M. Feck,

Kory J. Blose,

Lillian Assatourian,

David A. Vorp,

Patrick J. Pagano

Publication year - 2014

Publication title -

arteriosclerosis thrombosis and vascular biology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.007

H-Index - 270

eISSN - 1524-4636

pISSN - 1079-5642

DOI - 10.1161/atvbaha.114.304936

Subject(s) - vascular smooth muscle , nox1 , phenotype , biology , microbiology and biotechnology , smooth muscle , signal transduction , anatomy , endocrinology , gene , genetics , reactive oxygen species , nadph oxidase

Blood vessel hemodynamics have profound influences on function and structure of vascular cells. One of the main mechanical forces influencing vascular smooth muscle cells (VSMC) is cyclic stretch (CS). Increased CS stimulates reactive oxygen species (ROS) production in VSMC, leading to their dedifferentiation, yet the mechanisms involved are poorly understood. This study was designed to test the hypothesis that pathological CS stimulates NADPH oxidase isoform 1 (Nox1)-derived ROS via MEF2B, leading to VSMC dysfunction via a switch from a contractile to a synthetic phenotype.

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