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Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes
Published on: September 18, 2017
Regulatory volume decrease in cardiomyocytes is modulated by calcium influx and reactive oxygen species.
Diego Rojas-Rivera1, Jessica Díaz-Elizondo, Valentina Parra
1Centro FONDAP Estudios Moleculares de la Célula, Departamentos de, Santiago 838-0492, Chile.
FEBS Letters
|October 13, 2009
Summary
Hypoosmotic stress impacts cardiomyocyte viability through calcium (Ca2+). While Ca2+ influx aids cell survival by activating regulatory volume decrease (RVD), it also generates reactive oxygen species (ROS) that inhibit RVD and cause necrosis.
Area of Science:
- Cardiology
- Cell Physiology
- Biochemistry
Background:
- Cardiomyocytes face challenges from osmotic stress.
- Calcium ions (Ca2+) and reactive oxygen species (ROS) are implicated in cell volume regulation and survival.
Purpose of the Study:
- To investigate the role of Ca2+ in ROS generation under hyposmotic stress.
- To explore the relationship between Ca2+ influx, ROS, and regulatory volume decrease (RVD) in cardiomyocytes.
Main Methods:
- Utilized hyposmotic stress (Hypo) on cardiomyocytes.
- Administered nifedipine (Nife) to block Ca2+ channels.
- Overexpressed catalase (CAT) to assess ROS impact.
Main Results:
- Hypoosmotic stress increased both cytoplasmic and mitochondrial Ca2+.
- Nifedipine blocked Ca2+ influx and ROS generation.
- Catalase overexpression promoted RVD and reduced blebbing, but nifedipine abolished this effect.
Conclusions:
- Hypoosmotic stress has a dual effect on cardiomyocyte viability via Ca2+ influx.
- Ca2+ influx activates RVD for survival but also triggers ROS production, leading to necrosis.
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