ArticleAmerican journal of physiology. Lung cellular and molecular physiology2007
Cav3.1 (alpha1G) controls von Willebrand factor secretion in rat pulmonary microvascular endothelial cells.
Article in American journal of physiology. Lung cellular and molecular physiology, 2007. 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, 26 citations in OpenAlex.
- Voltage-Dependent Ion Channels in Vascular Endothelial Cells: An Unexpected Signaling Pathway in Non-Excitable Cells.Biomedicines · 2026Review
- CaJournal of thrombosis and haemostasis : JTH · 2022Article
- Mibefradil and Flunarizine, Two T-Type Calcium Channel Inhibitors, Protect Mice against Lipopolysaccharide-Induced Acute Lung Injury.Mediators of inflammation · 2020Article
- αAmerican journal of physiology. Cell physiology · 2019Article
- Ion Channels in Pulmonary Hypertension: A Therapeutic Interest?International journal of molecular sciences · 2018Review
- Transcriptional regulation of α1H T-type calcium channel under hypoxia.American journal of physiology. Cell physiology · 2014Article
- Regulation of cellular communication by signaling microdomains in the blood vessel wall.Pharmacological reviews · 2014Review
- Update on vascular endothelial Ca(2+) signalling: A tale of ion channels, pumps and transporters.World journal of biological chemistry · 2012Article
- Adenosine monophosphate-activated kinase alpha1 promotes endothelial barrier repair.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2011Article
- Altered protein kinase C regulation of pulmonary endothelial store- and receptor-operated Ca2+ entry after chronic hypoxia.The Journal of pharmacology and experimental therapeutics · 2010Article
- Alpha1G T-type calcium channel selectively regulates P-selectin surface expression in pulmonary capillary endothelium.American journal of physiology. Lung cellular and molecular physiology · 2010Article
- New developments in lung endothelial heterogeneity: Von Willebrand factor, P-selectin, and the Weibel-Palade body.Seminars in thrombosis and hemostasis · 2010Review
- Ca2+ entry via alpha1G and TRPV4 channels differentially regulates surface expression of P-selectin and barrier integrity in pulmonary capillary endothelium.American journal of physiology. Lung cellular and molecular physiology · 2009Article
- Effects of distension on airway inflammation and venular P-selectin expression.American journal of physiology. Lung cellular and molecular physiology · 2008Article
- Pulmonary expression of voltage-gated calcium channels: special reference to sensory airway receptors.Histochemistry and cell biology · 2007Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
Abstract
The T-type Ca2+ channel Cav3.1 subunit is present in pulmonary microvascular endothelial cells (PMVECs), but not in pulmonary artery endothelial cells (PAECs). The present study sought to assess the role of Cav3.1 in thrombin-induced Weibel-Palade body exocytosis and consequent von Willebrand factor (VWF) release. In PMVECs and PAECs transduced with a green fluorescent protein (GFP)-tagged VWF chimera, we examined the real-time dynamics and secretory process of VWF-GFP-containing vesicles in response to thrombin and the cAMP-elevating agent isoproterenol. Whereas thrombin stimulated a progressive decrease in the number of VWF-GFP-containing vesicles in both cell types, isoproterenol only decreased the number of VWF-GFP-containing vesicles in PAECs. In PMVECs, thrombin-induced decrease in the number of VWF-GFP-containing vesicles was nearly abolished by the T-type Ca2+ channel blocker mibefradil as well as by Cav3.1 gene silencing with small hairpin RNA. Expression of recombinant Cav3.1 subunit in PAECs resulted in pronounced increase in thrombin-stimulated Ca2+ entry, which is sensitive to mibefradil. Together, these data indicate that VWF secretion from lung endothelial cells is regulated by two distinct pathways involving Ca2+ or cAMP, and support the hypothesis that activation of Cav3.1 T-type Ca2+ channels in PMVECs provides a unique cytosolic Ca2+ source important for Gq-linked agonist-induced VWF release.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.