ArticleAmerican journal of physiology. Heart and circulatory physiology2009
Alternative splicing of Cav1.2 channel exons in smooth muscle cells of resistance-size arteries generates currents with unique electrophysiological properties.
Article in American journal of physiology. Heart and circulatory physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 39 citations in OpenAlex.
- The nonexcitable smooth muscle: remodeling the smooth muscle ion transport toolkit in disease.Physiological reviews · 2026Review
- Electric field stimulation unmasks a subtle role for T-type calcium channels in regulating lymphatic contraction.Scientific reports · 2023Article
- Electric field stimulation unmasks a subtle role for T-type calcium channels in regulating lymphatic contraction.Research square · 2023Article
- Oxidative Regulation of Vascular CaAntioxidants (Basel, Switzerland) · 2022Review
- Progressive aortic stiffness in aging C57Bl/6 mice displays altered contractile behaviour and extracellular matrix changes.Communications biology · 2022Article
- Post-Translational Modification of Cav1.2 and its Role in Neurodegenerative Diseases.Frontiers in pharmacology · 2021Review
- Alternative Splicing at N Terminus and Domain I Modulates CaBiophysical journal · 2018Article
- Characterization of CaChannels (Austin, Tex.) · 2018Article
- Smooth Muscle Ion Channels and Regulation of Vascular Tone in Resistance Arteries and Arterioles.Comprehensive Physiology · 2017Review
- Ion channel mechanisms of rat tail artery contraction-relaxation by menthol involving, respectively, TRPM8 activation and L-type Ca2+ channel inhibition.American journal of physiology. Heart and circulatory physiology · 2016Article
- Aberrant Splicing Promotes Proteasomal Degradation of L-type CaScientific reports · 2016Article
- Article
- The Physiology, Pathology, and Pharmacology of Voltage-Gated Calcium Channels and Their Future Therapeutic Potential.Pharmacological reviews · 2015Review
- Eugenol dilates rat cerebral arteries by inhibiting smooth muscle cell voltage-dependent calcium channels.Journal of cardiovascular pharmacology · 2014Article
- Ca(V)3.2 channels and the induction of negative feedback in cerebral arteries.Circulation research · 2014Article
- Should pharmacologists care about alternative splicing? IUPHAR Review 4.British journal of pharmacology · 2014Review
- A naturally occurring truncated Cav1.2 α1-subunit inhibits Ca2+ current in A7r5 cells.American journal of physiology. Cell physiology · 2013Article
- Developmental origins of colon smooth muscle dysfunction in IBS-like rats.American journal of physiology. Gastrointestinal and liver physiology · 2013Article
- The voltage-dependent L-type Ca2+ (CaV1.2) channel C-terminus fragment is a bi-modal vasodilator.The Journal of physiology · 2013Article
- Identification of L- and T-type Ca2+ channels in rat cerebral arteries: role in myogenic tone development.American journal of physiology. Heart and circulatory physiology · 2013Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Voltage-dependent calcium (Ca(2+), Ca(V)1.2) channels are the primary Ca(2+) entry pathway in smooth muscle cells of resistance-size (myogenic) arteries, but their molecular identity remains unclear. Here we identified and quantified Ca(V)1.2 alpha(1)-subunit splice variation in myocytes of rat resistance-size (100-200 microm diameter) cerebral arteries. Full-length clones containing either exon 1b or the recently identified exon 1c exhibited additional primary splice variation at exons 9*, 21/22, 31/32, and +/- 33. Real-time PCR confirmed the findings from full-length clones and indicated that the major Ca(V)1.2 variant contained exons 1c, 8, 21, and 32+33, with approximately 57% containing 9*. Exon 9* was more prevalent in clones containing 1c (72%) than in those containing 1b (33%), suggesting exon-selective combinatorial splicing. To examine the functional significance of this splicing profile, membrane currents produced by each of the four exon 1b/c/ +/- 9* variants were characterized following transfection in HEK293 cells. Exon 1c and 9* caused similar hyperpolarizing shifts in both current-voltage relationships and voltage-dependent activation of currents. Furthermore, exon 9* induced a hyperpolarizing shift only in the voltage-dependent activation of channels containing exon 1b, but not in those containing exon 1c. In contrast, exon 1b, 1c, or +9* did not alter voltage-dependent inactivation. In summary, we have identified the Ca(V)1.2 alpha(1)-subunit splice variant population that is expressed in myocytes of resistance-size arteries and the unique electrophysiological properties of recombinant channels formed by exon 1 and 9* variation. The predominance of exon 1c and 9* in smooth muscle cell Ca(V)1.2 channels causes a hyperpolarizing shift in the voltage sensitivity of currents toward the physiological arterial voltage range.
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