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CaV1.2 sparklets in heart and vascular smooth muscle
Manuel F Navedo1, Luis F Santana
1Department of Pharmacology, University of California, Davis, One Shields Ave., Davis, CA 95616, USA. mfnavedo@ucdavis.edu
Journal of Molecular and Cellular Cardiology
|December 11, 2012
Summary
CaV1.2 sparklets, crucial for muscle contraction, are regulated by protein kinases and phosphatases. AKAP150 anchors these enzymes, controlling calcium influx and strengthening excitation-contraction coupling in cardiac and smooth muscle.
Area of Science:
- Cardiovascular Physiology
- Molecular Cell Biology
- Muscle Contraction Mechanisms
Background:
- CaV1.2 sparklets are localized intracellular calcium (Ca2+) increases essential for excitation-contraction coupling in cardiac and arterial smooth muscle.
- Their activation is an early signaling event linking membrane depolarization to muscle contraction.
Purpose of the Study:
- To review the molecular and biophysical mechanisms regulating CaV1.2 sparklet activity.
- To discuss a model for local control of Ca2+ influx by signaling complexes.
Main Methods:
- Review of recent research on CaV1.2 channel regulation.
- Discussion of the role of protein kinases, phosphatases, and anchoring proteins.
Main Results:
- CaV1.2 sparklet activity is precisely controlled by protein kinases and phosphatases.
- The anchoring protein AKAP150 targets these enzymes to specific sarcolemmal regions.
- A signaling complex involving AKAP79/150, PKC, PKA, and calcineurin regulates CaV1.2 channels.
Conclusions:
- This signaling complex locally controls Ca2+ influx through CaV1.2 channels.
- Coordinated activation of CaV1.2 channel clusters amplifies Ca2+ influx.
- This amplification enhances excitation-contraction coupling in cardiac and vascular smooth muscle.
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