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Relaxin Modulates Fibroblast Function, Collagen Production, and Matrix Metalloproteinase‐2 Expression by Cardiac Fibroblasts
Author(s) -
MOOKERJEE ISHANEE,
UNEMORI ELAINE N.,
DU XIAOJUN,
TREGEAR GEOFFREY W.,
SAMUEL CHRISHAN S.
Publication year - 2005
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 - 10.1196/annals.1282.028
Subject(s) - relaxin , fibroblast , cardiac fibrosis , angiotensin ii , extracellular matrix , endocrinology , transforming growth factor , chemistry , matrix metalloproteinase , fibrosis , medicine , microbiology and biotechnology , receptor , biology , biochemistry , in vitro
A bstract : Cardiac fibrosis is a hallmark of heart disease and involves recruitment, proliferation, and differentiation of extracellular matrix‐producing fibroblasts, leading to overproduction of collagen within the myocardium. In this study, the effects of relaxin in inhibiting these processes were investigated. We used neonatal rat atrial and ventricular fibroblasts, which respond to pro‐fibrotic stimuli (i.e., transforming growth factor‐β and angiotensin II) and naturally express the relaxin receptor LGR7. Relaxin significantly inhibited TGF‐β‐ and angiotensin II‐mediated fibroblast function and collagen production over a 72‐h period, while increasing MMP‐2 expression and activity in the presence of both profibrotic factors (all P <.05). These studies demonstrate that relaxin may have therapeutic potential in diseased states characterized by cardiac fibrosis.