ArticleProceedings of the National Academy of Sciences of the United States of America2006
Atherosclerosis-related molecular alteration of the human CaV1.2 calcium channel alpha1C subunit.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 81 citations in OpenAlex.
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- An overview of potential molecular mechanisms involved in VSMC phenotypic modulation.Histochemistry and cell biology · 2016Review
- Effect of angiotensin II-induced arterial hypertension on the voltage-dependent contractions of mouse arteries.Pflugers Archiv : European journal of physiology · 2016Article
- Post-transcriptional modifications and "Calmodulation" of voltage-gated calcium channel function: Reflections by two collaborators of David T Yue.Channels (Austin, Tex.) · 2016Review
- Clinical Relevance of Serotonin Receptor Splice Variant Distribution in Human Colon.Journal of neurogastroenterology and motility · 2015Article
- Alternative splicing generates a novel truncated Cav1.2 channel in neonatal rat heart.The Journal of biological chemistry · 2015Article
- Calcium Channel CaVα₁ Splice Isoforms - Tissue Specificity and Drug Action.Current molecular pharmacology · 2015Review
- Should pharmacologists care about alternative splicing? IUPHAR Review 4.British journal of pharmacology · 2014Review
- RBFOX1 cooperates with MBNL1 to control splicing in muscle, including events altered in myotonic dystrophy type 1.PloS one · 2014Article
- Deletion of the insulin receptor in the proximal tubule promotes hyperglycemia.Journal of the American Society of Nephrology : JASN · 2013Article
- Effect of aging on calcium signaling in C57Bl6J mouse cerebral arteries.Pflugers Archiv : European journal of physiology · 2013Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Atherosclerosis is an inflammatory process characterized by proliferation and dedifferentiation of vascular smooth muscle cells (VSMC). Ca(v)1.2 calcium channels may have a role in atherosclerosis because they are essential for Ca(2+)-signal transduction in VSMC. The pore-forming Ca(v)1.2alpha1 subunit of the channel is subject to alternative splicing. Here, we investigated whether the Ca(v)1.2alpha1 splice variants are affected by atherosclerosis. VSMC were isolated by laser-capture microdissection from frozen sections of adjacent regions of arteries affected and not affected by atherosclerosis. In VSMC from nonatherosclerotic regions, RT-PCR analysis revealed an extended repertoire of Ca(v)1.2alpha1 transcripts characterized by the presence of exons 21 and 41A. In VSMC affected by atherosclerosis, expression of the Ca(v)1.2alpha1 transcript was reduced and the Ca(v)1.2alpha1 splice variants were replaced with the unique exon-22 isoform lacking exon 41A. Molecular remodeling of the Ca(v)1.2alpha1 subunits associated with atherosclerosis caused changes in electrophysiological properties of the channels, including the kinetics and voltage-dependence of inactivation, recovery from inactivation, and rundown of the Ca(2+) current. Consistent with the pathophysiological state of VSMC in atherosclerosis, cell culture data pointed to a potentially important association of the exon-22 isoform of Ca(v)1.2alpha1 with proliferation of VSMC. Our findings are consistent with a hypothesis that localized changes in cytokine expression generated by inflammation in atherosclerosis affect alternative splicing of the Ca(v)1.2alpha1 gene in the human artery that causes molecular and electrophysiological remodeling of Ca(v)1.2 calcium channels and possibly affects VSMC proliferation.
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