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Isolation of Human Myoblasts, Assessment of Myogenic Differentiation, and Store-operated Calcium Entry Measurement
Published on: July 26, 2017
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Store-Operated Calcium Entry in Mouse Cardiomyocytes
K O Gusev1, V V Vigont2, D A Grekhnev2
1Department of Ion Channels of Cell Membranes, Institute of Cytology, Russian Academy of Science, St. Petersburg, Russia. k.o.gusev@gmail.com.
Bulletin of Experimental Biology and Medicine
|July 27, 2019
Summary
Mature heart cells exhibit store-operated calcium entry, crucial for regulating calcium levels. Dysfunctional calcium entry in cardiomyocytes may contribute to heart disease development.
Area of Science:
- Cardiology
- Cell Physiology
- Molecular Biology
Background:
- Calcium ions (Ca2+) play critical roles in cardiac function, including excitation-contraction coupling.
- Endoplasmic reticulum Ca2+ stores are vital for maintaining cellular Ca2+ homeostasis.
- Store-operated calcium entry (SOCE) is a key mechanism for refilling intracellular Ca2+ stores.
Purpose of the Study:
- To investigate the presence and characteristics of store-operated calcium entry in mature ventricular cardiomyocytes.
- To determine the functional properties and pharmacological sensitivity of SOCE in these cells.
- To explore the potential link between SOCE dysfunction and heart disease.
Main Methods:
- Utilized the fluorescent dye fura-2 AM to monitor Ca2+ entry.
- Employed the whole-cell voltage clamp technique to record Ca2+ currents.
- Applied 2-aminoethoxydiphenyl borate (2-APB) to assess the sensitivity of Ca2+ currents to SOCE inhibitors.
Main Results:
- Identified Ca2+ currents activated by endoplasmic reticulum Ca2+ store depletion.
- Characterized these currents with amplitudes of 0.46±0.13 pA/pF and current-voltage relationships resembling classical CRAC channels.
- Demonstrated that these currents are inhibited by 2-APB (50 μM), confirming their nature as store-operated calcium entry.
Conclusions:
- Store-operated calcium entry is a significant feature of mature ventricular cardiomyocytes.
- SOCE in cardiomyocytes is mediated by channels with properties similar to CRAC channels.
- Alterations in SOCE may play a role in the pathogenesis of cardiac diseases, highlighting a potential therapeutic target.
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