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Angiotensin II activates programmed myocyte cell death in vitro
1Department of Medicine, New York Medical College, Valhalla 10595, USA.
Experimental Cell Research
|March 15, 1997
Summary
Angiotensin II (Ang II) triggers programmed cell death in neonatal heart cells by increasing intracellular calcium. This process involves AT1 receptor activation and calcium-dependent enzymes, leading to DNA damage.
Area of Science:
- Cardiology
- Molecular Biology
- Cell Biology
Background:
- Neonatal ventricular myocytes are crucial for heart development.
- Understanding triggers of myocyte cell death is vital for cardiovascular health.
Purpose of the Study:
- To investigate if angiotensin II (Ang II) induces apoptosis in neonatal ventricular myocytes.
- To elucidate the molecular mechanisms underlying Ang II-mediated myocyte apoptosis.
Main Methods:
- Neonatal rat ventricular myocytes were treated with Ang II in vitro.
- Apoptosis was assessed using TUNEL assay and DNA gel electrophoresis.
- Intracellular calcium levels and endonuclease activity were measured.
Main Results:
- Ang II significantly increased DNA double-strand cleavage and DNA fragmentation.
- Ang II elevated intracellular calcium levels and activated calcium-dependent endonuclease.
- AT1 receptor blockade (losartan) and calcium chelation (BAPTA-AM) inhibited Ang II-induced apoptosis.
Conclusions:
- Angiotensin II induces apoptosis in neonatal ventricular myocytes via AT1 receptor activation.
- Elevated cytosolic calcium and activated calcium-dependent endonuclease mediate this process.
- Targeting the AT1 receptor-calcium pathway may offer therapeutic strategies for preventing myocyte loss.