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Mechanical overload-induced apoptosis: a study in cultured neonatal ventricular myocytes and fibroblasts
Marion Persoon-Rothert1, Karlien G C van der Wees, Arnoud van der Laarse
1Department of Cardiology, Leiden University Medical Center, Leiden, The Netherlands.
Insights
Mechanical stretch did not directly induce apoptosis in cultured heart cells. This suggests that the complex 3D structure of the heart is crucial for stretch-induced cell death signaling.
Area of Science:
- Cardiovascular Biology
- Cell Death Mechanisms
Background:
- Cardiac myocyte apoptosis is linked to heart dysfunction from chronic hemodynamic overload.
- The role of apoptosis in heart failure progression remains unclear.
Purpose of the Study:
- To investigate the direct relationship between mechanical overload and apoptosis induction in an in vitro heart cell model.
- To determine if cyclic mechanical stretch triggers apoptosis in cardiac myocytes and fibroblasts.
Main Methods:
- Cultured neonatal rat ventricular myocytes and fibroblasts were subjected to cyclic mechanical stretch.
- Apoptosis was assessed using morphological changes, caspase-3 activity, and DNA fragmentation assays.
- Staurosporine was used as a positive control for apoptosis induction.
Main Results:
- Mechanical stretch did not induce significant apoptosis in cultured myocytes or fibroblasts.
- Staurosporine administration resulted in massive apoptosis in both cell types.
- The in vitro model did not demonstrate a direct link between mechanical stretch and apoptosis.
Conclusions:
- The tested in vitro cell model does not establish a direct causal link between mechanical stretch and apoptosis.
- The complex 3D structure and tissue interactions in the intact heart may be necessary for stretch-induced apoptotic signaling.
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.
