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The Extracellular Matrix Dynamically Regulates Smooth Muscle Cell Responsiveness to PDGF a
Author(s) -
RAINES ELAINE W.,
KOYAMA HIDENORI,
CARRAGHER NEIL O.
Publication year - 2000
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2000.tb06299.x
Subject(s) - extracellular matrix , fibronectin , integrin , microbiology and biotechnology , platelet derived growth factor receptor , platelet derived growth factor , chemistry , focal adhesion , growth factor , matrix (chemical analysis) , cytoskeleton , type i collagen , signal transduction , biology , cell , biochemistry , endocrinology , receptor , chromatography
A bstract : Focal accumulation of smooth muscle (SMC) within the arterial intima contributes to the formation of lesions of atherosclerosis. Platelet‐derived growth factor (PDGF) is a potent stimulant of SMC migration and proliferation in culture that may play a role in the accumulation of SMC in atherogenesis. SMCs normally reside in the media of the artery wall surrounded by extracellular matrix (ECM), including type I collagen. In atherogenesis, the ECM is degraded, new ECM components, such as fibronectin, are synthesized and assembled, and these alterations in ECM components are associated with changes in SMC phenotype. To model the changes in ECM in normal and diseased arteries, we have analyzed SMCs cultured on different forms of type I collagen. Our studies demonstrate that integrin‐mediated signals from various forms of type I collagen lead to specific and rapid modulation of the integrin signaling complex, including cytoskeletal connections, and of the responsiveness of SMC to PDGF stimulation.