ArticleThe Journal of biological chemistry2011
Ca(V)1.2 channel N-terminal splice variants modulate functional surface expression in resistance size artery smooth muscle cells.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 29 citations in OpenAlex.
- Mechanisms of Vascular CaHandbook of experimental pharmacology · 2023Article
- Progressive aortic stiffness in aging C57Bl/6 mice displays altered contractile behaviour and extracellular matrix changes.Communications biology · 2022Article
- Unveiling the Role of DNA Methylation in Vascular CACNA1C Tissue-Specific Expression.Frontiers in cardiovascular medicine · 2022Article
- Basal Vascular Smooth Muscle Cell Tone in eNOS Knockout Mice Can Be Reversed by Cyclic Stretch and Is Independent of Age.Frontiers in physiology · 2022Article
- A paradoxical increase of force development in saphenous and tail arteries from heterozygous ANO1 knockout mice.Physiological reports · 2020Article
- Alternative Splicing at N Terminus and Domain I Modulates CaBiophysical journal · 2018Article
- Alternative Splicing of L-type CaGenes · 2017Review
- Aberrant Splicing Promotes Proteasomal Degradation of L-type CaScientific reports · 2016Article
- The effect of trichostatin-A and tumor necrosis factor on expression of splice variants of the MaxiK and L-type channels in human myometrium.Frontiers in physiology · 2014Article
- A naturally occurring truncated Cav1.2 α1-subunit inhibits Ca2+ current in A7r5 cells.American journal of physiology. Cell physiology · 2013Article
- PKC independent inhibition of voltage gated calcium channels by volatile anesthetics in freshly isolated vascular myocytes from the aorta.Cell calcium · 2013Article
- Capturing single L-type Ca(2+) channel function with optics.Biochimica et biophysica acta · 2013Review
- The voltage-dependent L-type Ca2+ (CaV1.2) channel C-terminus fragment is a bi-modal vasodilator.The Journal of physiology · 2013Article
- Ion channel remodeling in vascular smooth muscle during hypertension: Implications for novel therapeutic approaches.Pharmacological research · 2013Review
- The calmodulin-binding, short linear motif, NSCaTE is conserved in L-type channel ancestors of vertebrate Cav1.2 and Cav1.3 channels.PloS one · 2013Article
- TMEM16A/ANO1 channels contribute to the myogenic response in cerebral arteries.Circulation research · 2012Article
- The Brugada syndrome mutation A39V does not affect surface expression of neuronal rat Cav1.2 channels.Molecular brain · 2012Article
- Levels of Ca(V)1.2 L-Type Ca(2+) Channels Peak in the First Two Weeks in Rat Hippocampus Whereas Ca(V)1.3 Channels Steadily Increase through Development.Journal of signal transduction · 2012Article
- TMEM16A channels generate Ca²⁺-activated Cl⁻ currents in cerebral artery smooth muscle cells.American journal of physiology. Heart and circulatory physiology · 2011Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Voltage-dependent Ca(2+) (Ca(V)1.2) channels are the primary Ca(2+) influx pathway in arterial smooth muscle cells and are essential for contractility regulation by a variety of stimuli, including intravascular pressure. Arterial smooth muscle cell Ca(V)1.2 mRNA is alternatively spliced at exon 1 (e1), generating e1b or e1c variants, with e1c exhibiting relatively smooth muscle-specific expression in the cardiovascular system. Here, we examined physiological functions of Ca(V)1.2e1 variants and tested the hypothesis that targeting Ca(V)1.2e1 modulates resistance size cerebral artery contractility. Custom antibodies that selectively recognize Ca(V)1.2 channel proteins containing sequences encoded by either e1b (Ca(V)1.2e1b) or e1c (Ca(V)1.2e1c) both detected Ca(V)1.2 in rat and human cerebral arteries. shRNA targeting e1b or e1c reduced expression of that Ca(V)1.2 variant, induced compensatory up-regulation of the other variant, decreased total Ca(V)1.2, and reduced intravascular pressure- and depolarization-induced vasoconstriction. Ca(V)1.2e1b and Ca(V)1.2e1c knockdown reduced whole cell Ca(V)1.2 currents, with Ca(V)1.2e1c knockdown most effectively reducing total Ca(V)1.2 and inducing the largest vasodilation. Knockdown of α(2)δ-1, a Ca(V)1.2 auxiliary subunit, reduced surface expression of both Ca(V)1.2e1 variants, inhibiting Ca(V)1.2e1c more than Ca(V)1.2e1b. e1b or e1c overexpression reduced Ca(V)1.2 surface expression and whole cell currents, leading to vasodilation, with e1c overexpression inducing the largest effect. In summary, data indicate that arterial smooth muscle cells express Ca(V)1.2 channels containing e1b or e1c-encoded N termini that contribute to Ca(V)1.2 surface expression, α(2)δ-1 preferentially traffics the Ca(V)1.2e1c variant to the plasma membrane, and targeting of Ca(V)1.2e1 message or the Ca(V)1.2 channel proximal N terminus induces vasodilation.
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Registered trials
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