Relaxin Modulates Fibroblast Function, Collagen Production, and Matrix Metalloproteinase-2 Expression by Cardiac Fibroblasts

: 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 investig...

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Bibliographic Details
Published in:Annals of the New York Academy of Sciences 2005-05, Vol.1041 (1), p.190-193
Main Authors: MOOKERJEE, ISHANEE, UNEMORI, ELAINE N., DU, XIAO-JUN, TREGEAR, GEOFFREY W., SAMUEL, CHRISHAN S.
Format: Article
Language:English
Subjects:
Angiotensin II - pharmacology
Animals
cardiac fibroblasts
Cell Differentiation - drug effects
Cell Proliferation - drug effects
Cells, Cultured
collagen
Collagen - biosynthesis
Collagen - secretion
Collagens
Differentiation
Enzyme Activation - drug effects
Fibroblasts
Fibroblasts - drug effects
Fibroblasts - physiology
Fibrosis
Gene Expression Regulation - drug effects
Heart - drug effects
Heart - secretion
Heart diseases
Matrix Metalloproteinase 2 - metabolism
matrix metalloproteinases
Myocardium - cytology
Myocardium - metabolism
Myocardium - secretion
Rats
Rats, Sprague-Dawley
Receptors
Recruitment
relaxin
Relaxin - pharmacology
Stimuli
Transforming Growth Factor beta - pharmacology
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Summary:: 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
ISSN:0077-8923
1749-6632
DOI:10.1196/annals.1282.028