期刊
MOLECULAR AND CELLULAR ENDOCRINOLOGY
卷 399, 期 C, 页码 9-21出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mce.2014.09.003
关键词
BNP; BMP-2; Cardiac myocyte; Hemodynamic stress; Mechanical stretch; Noggin
资金
- Medical Research Council of the Academy of Finland (Helsinki, Finland) [266661]
- Sigrid Juselius Foundation (Helsinki, Finland)
- Finnish Foundation for Cardiovascular Researh
- Paavo Ilmari Ahvenainen Foundation (Helsinki, Finland)
- Ida Montin Foundation (Espoo, Finland)
- Paulo Foundation (Helsinki, Finland)
- Research foundation of Pharmacal (Helsinki, Finland)
- Finnish Medical Society (Helsinki, Finland)
Hemodynamic overload exposes the heart to variety of neural, humoral and mechanical stresses. Even without the neurohumoral control of the entire organism cardiac myocytes have the ability to sense mechanical stretch and convert it into adaptive intracellular signals. This process is controlled by several growth factors. Here we show that mechanical stretch in vitro and hemodynamic overload in vivo activated the expression of bone morphogenetic protein-2 (BMP-2), while expression of BMP-4 was temporarily attenuated by stretch. BMP-2 and BMP-4 alone stimulated B-type and atrial natriuretic peptide (BNP and ANP) expression and protein synthesis, and activated transcription factor GATA-4 resembling the effects of mechanical stretch of cultured cardiac myocytes. Further, BMP antagonist Noggin was able to inhibit stretch and hypertrophic agonist induced BNP and ANP expression. Together these data provide evidence for BMP-2 as a new autocrine/paracrine factor that regulates cardiomyocyte mechanotransduction and adaptation to increased mechanical stretch. (C) 2014 Elsevier Ireland Ltd. All rights reserved.
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