ArticleAmerican journal of physiology. Cell physiology2011
Regulation and function of Cav3.1 T-type calcium channels in IGF-I-stimulated pulmonary artery smooth muscle cells.
Article in American journal of physiology. Cell physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 29 citations in OpenAlex.
- The nonexcitable smooth muscle: remodeling the smooth muscle ion transport toolkit in disease.Physiological reviews · 2026Review
- Insulin-like growth factor family and its impact on pulmonary arterial hypertension: a review.Frontiers in physiology · 2025Review
- EndothelialInternational journal of medical sciences · 2025Article
- Stimulated phosphorylation of ERK in mouse kidney mesangial cells is dependent upon expression of Cav3.1.BMC nephrology · 2022Article
- miR-137 and its target T-type CaCell proliferation · 2020Article
- Elementary calcium signaling in arterial smooth muscle.Channels (Austin, Tex.) · 2019Review
- Contribution of S4 segments and S4-S5 linkers to the low-voltage activation properties of T-type CaV3.3 channels.PloS one · 2018Article
- Heme oxygenase-1 regulates cell proliferation via carbon monoxide-mediated inhibition of T-type Ca2+ channels.Pflugers Archiv : European journal of physiology · 2015Article
- Deficiency of Akt1, but not Akt2, attenuates the development of pulmonary hypertension.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- Cav3.2 T-type calcium channel is required for the NFAT-dependent Sox9 expression in tracheal cartilage.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Regulation of ca(2+) signaling in pulmonary hypertension.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2013Article
- Benidipine protects kidney through inhibiting ROCK1 activity and reducing the epithelium-mesenchymal transdifferentiation in type 1 diabetic rats.Journal of diabetes research · 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
- 1,4-dihydropyridines: the multiple personalities of a blockbuster drug family.Translational medicine @ UniSa · 2012Article
- Depolarization-dependent contraction increase after birth and preservation following long-term hypoxia in sheep pulmonary arteries.Pulmonary circulationArticle
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Authors and funding
2 authors at 1 institution in 1 country.
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Abstract
Arterial smooth muscle cells enter the cell cycle and proliferate in conditions of disease and injury, leading to adverse vessel remodeling. In the pulmonary vasculature, diverse stimuli cause proliferation of pulmonary artery smooth muscle cells (PASMCs), pulmonary artery remodeling, and the clinical condition of pulmonary hypertension associated with significant health consequences. PASMC proliferation requires extracellular Ca(2+) influx that is intimately linked with intracellular Ca(2+) homeostasis. Among the primary sources of Ca(2+) influx in PASMCs is the low-voltage-activated family of T-type Ca(2+) channels; however, up to now, mechanisms for the action of T-type channels in vascular smooth muscle cell proliferation have not been addressed. The Ca(v)3.1 T-type Ca(2+) channel mRNA is upregulated in cultured PASMCs stimulated to proliferate with insulin-like growth factor-I (IGF-I), and this upregulation depends on phosphatidylinositol 3-kinase/Akt signaling. Multiple stimuli that trigger an acute rise in intracellular Ca(2+) in PASMCs, including IGF-I, also require the expression of Ca(v)3.1 Ca(2+) channels for their action. IGF-I also led to cell cycle initiation and proliferation of PASMCs, and, when expression of the Ca(v)3.1 Ca(2+) channel was knocked down by RNA interference, so were the expression and activation of cyclin D, which are necessary steps for cell cycle progression. These results confirm the importance of T-type Ca(2+) channels in proper progression of the cell cycle in PASMCs stimulated to proliferate by IGF-I and suggest that Ca(2+) entry through Ca(v)3.1 T-type channels in particular interacts with Ca(2+)-dependent steps of the mitogenic signaling cascade as a central component of vascular remodeling in disease.
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