Discoidin Domain Receptor-1 Regulates Calcific Extracellular Vesicle Release in Vascular Smooth Muscle Cell Fibrocalcific Response via Transforming Growth Factor-β Signaling
Author(s) -
Jona B. Krohn,
Joshua D. Hutcheson,
Eduardo MartínezMartínez,
Whitney S. Irvin,
Carlijn V. C. Bouten,
Sérgio Bertazzo,
Michelle P. Bendeck,
Elena Aïkawa
Publication year - 2016
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.115.307009
Subject(s) - vascular smooth muscle , ddr1 , microbiology and biotechnology , extracellular , transforming growth factor , discoidin domain , growth factor , signal transduction , extracellular vesicles , receptor , cell growth , chemistry , biology , anatomy , smooth muscle , endocrinology , medicine , biochemistry , receptor tyrosine kinase
Collagen accumulation and calcification are major determinants of atherosclerotic plaque stability. Extracellular vesicle (EV)-derived microcalcifications in the collagen-poor fibrous cap may promote plaque rupture. In this study, we hypothesize that the collagen receptor discoidin domain receptor-1 (DDR-1) regulates collagen deposition and release of calcifying EVs by vascular smooth muscle cells (SMCs) through the transforming growth factor-β (TGF-β) pathway.
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