期刊
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
卷 42, 期 2, 页码 367-377出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.yjmcc.2006.11.002
关键词
inflammation; hypertrophy; integrin; signaling; bone marrow transplant
资金
- NHLBI NIH HHS [HL 076670, HL 061567, HL 057278] Funding Source: Medline
- NIDDK NIH HHS [P30 DK 52574] Funding Source: Medline
Cardiac hypertrophy commonly develops in response to pressure overload and is associated with increased mortality. Mechanical stress in the heart can result in the activation of transmembrane integrin alpha beta heterodimers that are expressed in cardiomyocytes. Once activated, integrins stimulate focal adhesion kinase, Grb2, c-src, and other signaling molecules to promote cardiomyocyte growth and gene expression. Mechanical stress can also promote cardiac inflammation that may be mediated, in part, by the activation of integrins expressed in blood-borne cells. To address the role of one integrin, beta(3), in the pathogenesis of cardiac hypertrophy, beta(-/-)(3) mice were examined. beta(-/-)(3) Mice developed moderate spontaneous cardiac hypertrophy associated with systolic and diastolic dysfunction, and these abnormalities were exacerbated by transverse aortic constriction, In addition, beta(-/-)(3) mice developed mild cardiac inflammation with infiltrating macrophages at baseline that was markedly worsened by pressure overload. Bone marrow transplantation experiments showed that blood-borne cells were at least partially responsible for the cardiac hypertrophy and inflammation observed in beta(-/-)(3) mice. These results suggest that alpha(v)beta(3) expression in bone marrow has a generalized suppressive effect on cardiac inflammation. (c) 2006 Elsevier Inc. All rights reserved.
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