Published online before print May 19, 2003, doi: 10.1161/01.HYP.0000074905.22908.A6
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(Hypertension. 2003;42:88.)
© 2003 American Heart Association, Inc.
Scientific Contributions |
Effects of Pressure Overload on Extracellular Matrix Expression in the Heart of the Atrial Natriuretic Peptide–Null Mouse
From the Vascular Biology and Hypertension Program, Division of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham (D.W., S.O., J.A.F., P.L. G.P., Y.-F.C.); the Cardiology Section, Birmingham VA Medical Center (G.P.), Birmingham, Ala; the Department of Cancer Biology, Dana-Farber Cancer Institute, Harvard Medical School (L.B.C., M.D.), Boston, Mass; and the Howard Hughes Medical Institute and Jackson Laboratory (S.W.M.J.), Bar Harbor, Me.
Correspondence to Yiu-Fai Chen, PhD, 1008 ZRB, Vascular Biology and Hypertension Program, University of Alabama at Birmingham, Birmingham, AL 35294. E-mail yfchen{at}uab.edu
This study tested the hypothesis that atrial natriuretic peptide has direct antihypertrophic actions on the heart by modulating expression of genes involved in cardiac hypertrophy and extracellular matrix production. Hearts of male, atrial natriuretic peptide–null and control wild-type mice that had been subjected to pressure overload after transverse aortic constriction and control unoperated hearts were weighed and subjected to microarray, Northern blot, and immunohistochemical analyses. Microarray and Northern blot analyses were used to identify genes that are regulated differentially in response to stress in the presence and absence of atrial natriuretic peptide. Immunohistochemical analysis was used to identify and localize expression of the protein products of these genes. Atrial natriuretic peptide–null mice demonstrated cardiac hypertrophy at baseline and an exaggerated hypertrophic response to transverse aortic constriction associated with increased expression of the extracellular matrix molecules periostin, osteopontin, collagen I and III, and thrombospondin, as well as the extracellular matrix regulatory proteins, matrix metalloproteinase-2 and tissue inhibitor of metalloproteinase-3, and the novel growth factor pleiotrophin compared with wild-type controls. These results support the hypothesis that atrial natriuretic peptide protects against pressure overload–induced cardiac hypertrophy and remodeling by negative modulation of genes involved in extracellular matrix deposition.
Key Words: atrial natriuretic factor • constriction • aorta • pressure overload • hypertrophy, cardiac • extracellular matrix • growth substances
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