ArticleAmerican journal of physiology. Cell physiology2008
Ca2+ handling is altered when arterial myocytes progress from a contractile to a proliferative phenotype in culture.
Article in American journal of physiology. Cell physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers.
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Who cites it
116 citing papers in PubMed, 192 citations in OpenAlex.
- The nonexcitable smooth muscle: remodeling the smooth muscle ion transport toolkit in disease.Physiological reviews · 2026Review
- Aldosterone increases the expression and subcellular localization of SERCA2a and SERCA2b in the rat mesenteric artery.Frontiers in physiology · 2026Article
- The machinery of healthy vasoconstriction: an overview.Pflugers Archiv : European journal of physiology · 2025Review
- The role and mechanism of vascular wall cell ion channels in vascular fibrosis remodeling.Channels (Austin, Tex.) · 2024Review
- Endothelial cell Orai1 is essential for endothelium-dependent contraction of mouse carotid arteries in normotensive and hypertensive mice.Acta pharmacologica Sinica · 2024Article
- Alterations of the CaFrontiers in physiology · 2023Article
- STIM1 is a core trigger of airway smooth muscle remodeling and hyperresponsiveness in asthma.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- The mechanosensitive Piezo1 channels contribute to the arterial medial calcification.Frontiers in physiology · 2022Article
- Ion Channels and Transporters in Muscle Cell Differentiation.International journal of molecular sciences · 2021Review
- Article
- Role of Airway Smooth Muscle in Inflammation Related to Asthma and COPD.Advances in experimental medicine and biology · 2021Article
- Store-Operated Calcium Entry in the Cardiovascular System.Advances in experimental medicine and biology · 2021Review
- Enhanced Store-Operated CaFrontiers in physiology · 2021Article
- On a Magical Mystery Tour with 8-Bromo-Cyclic ADP-Ribose: From All-or-None Block to Nanojunctions and the Cell-Wide Web.Molecules (Basel, Switzerland) · 2020Review
- Obligatory role for PKCδ in PIPThe Journal of physiology · 2020Article
- TRPC and TRPV Channels' Role in Vascular Remodeling and Disease.International journal of molecular sciences · 2020Review
- L-type CaProceedings of the National Academy of Sciences of the United States of America · 2020Article
- Reduced CaAging · 2020Article
- Insights into Activation Mechanisms of Store-Operated TRPC1 Channels in Vascular Smooth Muscle.Cells · 2020Review
- Article
56 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Phenotypic modulation of vascular myocytes is important for vascular development and adaptation. A characteristic feature of this process is alteration in intracellular Ca(2+) handling, which is not completely understood. We studied mechanisms involved in functional changes of inositol 1,4,5-trisphosphate (IP(3))- and ryanodine (Ry)-sensitive Ca(2+) stores, store-operated Ca(2+) entry (SOCE), and receptor-operated Ca(2+) entry (ROCE) associated with arterial myocyte modulation from a contractile to a proliferative phenotype in culture. Proliferating, cultured myocytes from rat mesenteric artery have elevated resting cytosolic Ca(2+) levels and increased IP(3)-sensitive Ca(2+) store content. ATP- and cyclopiazonic acid [CPA; a sarco(endo)plasmic reticulum Ca(2+)-ATPase (SERCA) inhibitor]-induced Ca(2+) transients in Ca(2+)-free medium are significantly larger in proliferating arterial smooth muscle cells (ASMCs) than in freshly dissociated myocytes, whereas caffeine (Caf)-induced Ca(2+) release is much smaller. Moreover, the Caf/Ry-sensitive store gradually loses sensitivity to Caf activation during cell culture. These changes can be explained by increased expression of all three IP(3) receptors and a switch from Ry receptor type II to type III expression during proliferation. SOCE, activated by depletion of the IP(3)/CPA-sensitive store, is greatly increased in proliferating ASMCs. Augmented SOCE and ROCE (activated by the diacylglycerol analog 1-oleoyl-2-acetyl-sn-glycerol) in proliferating myocytes can be attributed to upregulated expression of, respectively, transient receptor potential proteins TRPC1/4/5 and TRPC3/6. Moreover, stromal interacting molecule 1 (STIM1) and Orai proteins are upregulated in proliferating cells. Increased expression of IP(3) receptors, SERCA2b, TRPCs, Orai(s), and STIM1 in proliferating ASMCs suggests that these proteins play a critical role in an altered Ca(2+) handling that occurs during vascular growth and remodeling.
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