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Sarcoplasmic reticulum Ca(2+)ATPase and cell contraction in developing rabbit heart.
1Department of Pediatrics, University of California Los Angeles, Los Angeles, California, USA.
Journal of Molecular and Cellular Cardiology
|April 25, 2000
Summary
Immature rabbit hearts have sufficient sarcoplasmic reticulum Ca(2+)-ATPase (SERCA2a) expression and function. This indicates that SERCA2a maturity is not the cause of reduced SR Ca(2+) release in young hearts.
Area of Science:
- Cardiovascular Physiology
- Molecular Cardiology
- Cell Biology
Background:
- Cardiac function matures postnatally.
- Sarcoplasmic reticulum Ca(2+)-ATPase (SERCA2a) is crucial for cardiac muscle relaxation.
- Age-related changes in SERCA2a may impact cardiac contractility.
Purpose of the Study:
- To investigate age-related changes in cardiac SERCA2a expression and function.
- To determine if SERCA2a immaturity contributes to reduced SR Ca(2+) release in immature hearts.
Main Methods:
- Quantitative analysis of SERCA2a protein levels and localization in rabbit hearts at different developmental stages (fetal, neonatal, juvenile, adult).
- In situ functional assessment of SERCA in isolated cardiac myocytes by measuring SR Ca(2+) store reloading rates after caffeine-induced depletion.
Main Results:
- Significant SERCA2a expression is present early in immature hearts, reaching adult levels within 15-30 days post-birth.
- SERCA2a protein exhibits transverse striations within myocytes from 1 day of age.
- In situ SERCA function in neonatal and adult myocytes is comparable in maintaining SR Ca(2+) stores.
Conclusions:
- Immature cardiac myocytes do not exhibit a paucity of SERCA2a expression.
- The reduced SR Ca(2+) release observed in immature ventricular myocytes is not attributable to SERCA2a immaturity.