| Enhanced store-operated Ca²+ entry and TRPC channel expression in pulmonary arteries of monocrotaline-induced pulmonary hypertensive rats. | |
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MedLine Citation:
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PMID: 21940663 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Pulmonary hypertension (PH) is associated with profound vascular remodeling and alterations in Ca(2+) homeostasis in pulmonary arterial smooth muscle cells (PASMCs). Previous studies show that canonical transient receptor potential (TRPC) genes are upregulated and store-operated Ca(2+) entry (SOCE) is augmented in PASMCs of chronic hypoxic rats and patients of pulmonary arterial hypertension (PAH). Here we further examine the involvement of TRPC and SOCE in PH with a widely used rat model of monocrotaline (MCT)-induced PAH. Rats developed severe PAH, right ventricular hypertrophy, and significant increase in store-operated TRPC1 and TRPC4 mRNA and protein in endothelium-denuded pulmonary arteries (PAs) 3 wk after MCT injection. Contraction of PA and Ca(2+) influx in PASMC evoked by store depletion using cyclopiazonic acid (CPA) were enhanced dramatically, consistent with augmented SOCE in the MCT-treated group. The time course of increase in CPA-induced contraction corresponded to that of TRPC1 expression. Endothelin-1 (ET-1)-induced vasoconstriction was also potentiated in PAs of MCT-treated rats. The response was partially inhibited by SOCE blockers, including Gd(3+), La(3+), and SKF-96365, as well as the general TRPC inhibitor BTP-2, suggesting that TRPC-dependent SOCE was involved. Moreover, the ET-1-induced contraction and Ca(2+) response in the MCT group were more susceptible to the inhibition caused by the various SOCE blockers. Hence, our study shows that MCT-induced PAH is associated with increased TRPC expression and SOCE, which are involved in the enhanced vascular reactivity to ET-1, and support the hypothesis that TRPC-dependent SOCE is an important pathway for the development of PH. |
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Authors:
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Xiao-Ru Liu; Ming-Fang Zhang; Na Yang; Qing Liu; Rui-Xing Wang; Yuan-Ning Cao; Xiao-Ru Yang; James S K Sham; Mo-Jun Lin |
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Publication Detail:
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Type: Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2011-09-21 |
Journal Detail:
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Title: American journal of physiology. Cell physiology Volume: 302 ISSN: 1522-1563 ISO Abbreviation: Am. J. Physiol., Cell Physiol. Publication Date: 2012 Jan |
Date Detail:
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Created Date: 2011-12-19 Completed Date: 2012-02-06 Revised Date: 2013-02-20 |
Medline Journal Info:
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Nlm Unique ID: 100901225 Medline TA: Am J Physiol Cell Physiol Country: United States |
Other Details:
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Languages: eng Pagination: C77-87 Citation Subset: IM |
Affiliation:
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Department of Physiology and Pathophysiology, Fujian Medical University, Fuzhou, Fujian Province, People's Republic of China. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Calcium / metabolism, physiology Calcium Signaling / physiology* Cells, Cultured Hypertension, Pulmonary / chemically induced, metabolism* Male Monocrotaline / administration & dosage* Organ Culture Techniques Pulmonary Artery / drug effects, metabolism* Rats Rats, Sprague-Dawley TRPC Cation Channels / biosynthesis*, physiology |
| Grant Support | |
ID/Acronym/Agency:
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R01-HL-071835/HL/NHLBI NIH HHS; R01-HL-075134/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/TRPC Cation Channels; 0/TRPC4 ion channel; 0/transient receptor potential cation channel, subfamily C, member 1; 315-22-0/Monocrotaline; 7440-70-2/Calcium |
| Comments/Corrections | |
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