© 2005 European Society of Cardiology
Mechanical stretch-induced hypertrophy of neonatal rat ventricular myocytes is mediated by β1-integrin-microtubule signaling pathways
Cardiology Department of No.1 Hospital of Xi'an Jiaotong University 1 Jiankang Road, Xi'an, Shaanxi, China Key Laboratory of Environment and Genes Related to Diseases (Xi'an Jiaotong University), Ministry of Education Xi'an, Shaanxi 710061, China
* Corresponding author. Tel.: +86 29 85261809; fax: +86 29 85396990. E-mail address: maaiqun{at}medmail.com.cn
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Abstract |
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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 µmol/ml) and anti-integrin β1 specific antibody (10 µg/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 β1 blocking antibody effectively inhibited the increase in 3H-leucine incorporation and release of ANP (p<0.05). Following anti-integrin-β1-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-β1-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.
Key Words: Mechanical stretch • β1-integrin • Microtubule • Cardiomyocyte • Hypertrophy
Received December 8, 2004; Accepted May 25, 2005
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