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Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes
Published on: September 18, 2017
Defective Ca(2+) handling proteins regulation during heart failure
1Department of Biophysics, Second Military Medical University, Shanghai, People's Republic of China.
Physiological Research
|October 16, 2010
Summary
Heart failure in rats shows reduced sarcoplasmic reticulum calcium levels and impaired calcium handling proteins. This dysfunction contributes to cardiac issues by affecting calcium release, uptake, and extrusion.
Area of Science:
- Cardiology
- Molecular Biology
- Physiology
Background:
- Abnormal calcium (Ca2+) release from the sarcoplasmic reticulum (SR) via the cardiac ryanodine receptor (RyR2) is implicated in heart failure (HF) contractile dysfunction.
- Previous studies indicated reduced FK506 binding protein (FKBP12.6) in RyR2 complexes from HF rat hearts.
Purpose of the Study:
- To investigate the expression of key Ca2+ handling proteins and SR Ca2+ content in rat cardiac myocytes from control and HF models.
- To elucidate the molecular mechanisms underlying Ca2+ dysregulation in HF.
Main Methods:
- Direct measurement of SR Ca2+ content in permeabilized cardiac myocytes.
- Assessment of the expression levels of RyR2-associated proteins, SERCA2a, PLB phosphorylation (Ser16, Thr17), Cav1.2, and NCX in control and HF rat myocytes.
Main Results:
- SR luminal Ca2+ content was significantly lower in HF myocytes compared to controls.
- Expression of RyR2-associated proteins, SERCA2a, PLB-S16, PLB-T17, Cav1.2, and NCX were all significantly reduced in HF rats.
- Defective protein-protein interactions within RyR2 macromolecular complexes were observed.
Conclusions:
- Reduced SR Ca2+ content and impaired Ca2+ handling contribute to HF.
- Dysregulation of Ca2+ release, uptake, and extrusion mechanisms, including defective RyR2-RyR2 protein interactions, play a critical role in HF pathophysiology.
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