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Optical Mapping of Intra-Sarcoplasmic Reticulum Ca2+ and Transmembrane Potential in the Langendorff-perfused Rabbit Heart
Published on: September 10, 2015
Sorcin modulates cardiac L-type Ca2+ current by functional interaction with the alpha1C subunit in rabbits
Mark R Fowler1, Gianni Colotti, Emilia Chiancone
1Faculty of Biomedical & Life Sciences, West Medical Building, University of Glasgow, Glasgow G12 8QQ, UK.
Experimental Physiology
|July 8, 2008
Summary
Sorcin, a regulatory protein, directly modulates cardiac L-type calcium channels (LTCCs). This interaction alters ion channel function, with effects varying based on experimental conditions and charge carriers used.
Area of Science:
- Cardiovascular Physiology
- Molecular Cardiology
- Ion Channel Biophysics
Background:
- Cardiac L-type Ca(2+) channels (LTCCs) are crucial for heart function.
- Sorcin is a known regulatory protein with potential roles in cellular signaling.
Purpose of the Study:
- To investigate the direct interaction between sorcin and cardiac LTCCs.
- To determine how sorcin modulates LTCC function.
Main Methods:
- Whole-cell patch-clamp recordings were performed on native rabbit ventricular myocytes.
- HEK 293 cells expressing cardiac alpha(1C) subunits were utilized.
- Experiments used Ca(2+) or Ba(2+) as charge carriers.
Main Results:
- Sorcin increased peak current in ventricular myocytes with both Ca(2+) and Ba(2+).
- In HEK 293 cells, sorcin increased peak current density with Ba(2+) but not Ca(2+).
- Sorcin altered current inactivation kinetics (tau(fast)) differently depending on the charge carrier and cell type.
Conclusions:
- Sorcin directly interacts with LTCCs, primarily via its C-terminal domain.
- This interaction modifies LTCC current magnitude and inactivation kinetics.
- The observed modulatory effects are influenced by experimental conditions and charge carriers.
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