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Eur J Heart Fail. 2006 Jan;8(1):16-22. Epub 2005 Sep 29.

Mechanical stretch-induced hypertrophy of neonatal rat ventricular myocytes is mediated by beta(1)-integrin-microtubule signaling pathways.

Author information

1
Cardiology Department of No.1 Hospital of Xi'an Jiaotong University, 1 Jiankang Road, Xi'an, Shaanxi, China.

Abstract

BACKGROUND:

Mechanical stress plays a crucial role in tissue morphogenesis and remodeling. These processes depend in part on force transmission mediated through integrins and the cytoskeleton.

METHODS:

Ventricular myocytes isolated from neonatal Sprague-Dawley rats (NRVMs) were exposed to persistent centrifugal force stretch for 12 or 24 h. The NRVMs were exposed to colchicine (4 micromol/ml) and anti-integrin beta1 specific antibody (10 microg/ml). Cell viability was assessed by MTT assay and lactate dehydrogenase (LDH) activity. Incorporation of 3H-leucine, and atrial natriuretic peptide (ANP) and angiotensin II (Ang II) levels were assessed. Pixel intensity and distribution of the microtubule were estimated from laser scanning confocal images.

RESULTS:

Changes in LDH release and the MTT assay showed that 180 rpm. centrifugal force had minimal effect on the viability and number of NRVMs. Mechanical stretch significantly increased 3H-leucine incorporation into cardiomyocytes. Anti-integrin beta1 blocking antibody effectively inhibited the increase in 3H-leucine incorporation and release of ANP (p < 0.05). Following anti-integrin-beta1-blocking antibody, the pixel intensity of the microtubule image was decreased after both12 and 24 h stretch, this was similar to the effect of colchicine. Both treatments also inhibited the secretion of Ang II induced by stretch (p < 0.05).

CONCLUSIONS:

Anti-integrin-beta1-blocking antibody and colchicine had similar effects, partly inhibiting the stretch-induced increase in microtubule polymerization and the secretion of Ang II in hypertrophic cardiac myocytes.

PMID:
16198630
DOI:
10.1016/j.ejheart.2005.05.014
[Indexed for MEDLINE]
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