ArticleMolecular and cellular biochemistry2002
Mechanical overload-induced apoptosis: a study in cultured neonatal ventricular myocytes and fibroblasts.
Article in Molecular and cellular biochemistry, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Guanxinning tablets improve myocardial hypertrophy by inhibiting the activation of MEK-ERK1/2 signaling pathway.Journal of applied biomedicine · 2023Article
- The effects of cardiac stretch on atrial fibroblasts: analysis of the evidence and potential role in atrial fibrillation.Cardiovascular research · 2022Review
- Ivabradine improved left ventricular function and pressure overload-induced cardiomyocyte apoptosis in a transverse aortic constriction mouse model.Molecular and cellular biochemistry · 2019Article
- Persistence of apoptosis and inflammatory responses in the heart and bone marrow of mice following whole-body exposure to ²⁸Silicon (²⁸Si) ions.Radiation and environmental biophysics · 2013Article
- In vitro modeling of repetitive motion injury and myofascial release.Journal of bodywork and movement therapies · 2010Article
- Release of cardiac troponin I from viable cardiomyocytes is mediated by integrin stimulation.Pflugers Archiv : European journal of physiology · 2008Article
- Cellular stress failure in ventilator-injured lungs.American journal of respiratory and critical care medicine · 2005Review
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Authors and funding
3 authors.
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Abstract
Apoptosis of cardiac myocytes has been implicated in cardiac dysfunction due to chronic hemodynamic overload. Reports on the role of apoptosis in the transition from hypertrophy to decompensated heart failure are not unequivocal. In this study we analysed the direct relationship between mechanical overload and induction of apoptosis in an in vitro model of cultured heart cells. Cyclic mechanical stretch was applied to cultured neonatal rat ventricular myocytes and fibroblasts. Several indicators of apoptosis were examined, such as morphological features, caspase-3 activity and DNA fragmentation. Mechanical strain did not induce any significant change in these parameters as compared to non-stretched myocytes or fibroblasts. However, administration of staurosporine, a known inducer of apoptosis, induced massive apoptosis in myocytes as well as fibroblasts. We conclude that this in vitro cell model system lacks a direct link between mechanical stretch and apoptosis. The three-dimensional structure-function relationship of myocardial tissue in the intact heart may elicit stretch-induced molecular signaling cascades in a much more complex way than in monolayer cultures of cardiac cells.
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