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Rap 1a small GTPase alters extracellular matrix (ECM) deposition in response to TGF‐β1
Author(s) -
Jeyaraj Selvi C,
Unger Nicholas T,
Stewart James A,
Chotani Maqsood A
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1133.4
Subject(s) - extracellular matrix , fibrosis , microbiology and biotechnology , transforming growth factor , fibroblast , chemistry , cardiac fibrosis , endocrinology , myofibroblast , medicine , biology , biochemistry , in vitro
Cardiac fibroblasts are essential to cardiac remodeling by regulating ECM production, maturation and degradation. TGF‐β, transforming growth factor beta, can regulate fibroblast differentiation and activation, and therefore tissue fibrosis. Rap1a, a Ras‐like GTPase, has been implicated in cell migration and attachment, however, its role in regulation of ECM has yet to be determined. In this study, we examined the impact of Rap1 deficiency on cardiac ECM remodeling. Analysis of left ventricular tissue sections from Rap1a deficient heterozygous or knockout (HET or KO) mice revealed significant decreases in total (picrosirius red‐PASR), soluble and insoluble collagen when compared to wild‐type (WT) controls (Table I). Isolated cardiac fibroblasts from heterozygous Rap1a mice showed a blunted collagen response to TGF‐β, suggesting an alteration in the normal pro‐fibrotic response to this cytokine. Genetic ablation of Rap1a shows an impact on regulation of ECM which may lead to alterations in cardiac remodeling and hypertrophic response.