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dc.contributor.author
Yeon, Soo-In
dc.contributor.author
Kim, Joo Young
dc.contributor.author
Yeon, Dong-Soo
dc.contributor.author
Abramowitz, Joel
dc.contributor.author
Birnbaumer, Lutz
dc.contributor.author
Muallem, Shmuel
dc.contributor.author
Lee, Young-Ho
dc.date.available
2020-01-28T20:23:27Z
dc.date.issued
2014-10
dc.identifier.citation
Yeon, Soo-In; Kim, Joo Young; Yeon, Dong-Soo; Abramowitz, Joel; Birnbaumer, Lutz; et al.; Transient receptor potential canonical type 3 channels control the vascular contractility of mouse mesenteric arteries; Public Library of Science; Plos One; 9; 10; 10-2014; 1-9
dc.identifier.issn
1932-6203
dc.identifier.uri
http://hdl.handle.net/11336/96060
dc.description.abstract
Transient receptor potential canonical type 3 (TRPC3) channels are non-selective cation channels and regulate intracellular Ca2+ concentration. We examined the role of TRPC3 channels in agonist-, membrane depolarization (high K+)-, and mechanical (pressure)-induced vasoconstriction and vasorelaxation in mouse mesenteric arteries. Vasoconstriction and vasorelaxation of endothelial cells intact mesenteric arteries were measured in TRPC3 wild-type (WT) and knockout (KO) mice. Calcium concentration ([Ca2+]) was measured in isolated arteries from TRPC3 WT and KO mice as well as in the mouse endothelial cell line bEnd.3. Nitric oxide (NO) production and nitrate/nitrite concentrations were also measured in TRPC3 WT and KO mice. Phenylephrine-induced vasoconstriction was reduced in TRPC3 KO mice when compared to that of WT mice, but neither high K+- nor pressure-induced vasoconstriction was altered in TRPC3 KO mice. Acetylcholine-induced vasorelaxation was inhibited in TRPC3 KO mice and by the selective TRPC3 blocker pyrazole-3. Acetylcholine blocked the phenylephrine-induced increase in Ca2+ ratio and then relaxation in TRPC3 WT mice but had little effect on those outcomes in KO mice. Acetylcholine evoked a Ca2+ increase in endothelial cells, which was inhibited by pyrazole-3. Acetylcholine induced increased NO release in TRPC3 WT mice, but not in KO mice. Acetylcholine also increased the nitrate/nitrite concentration in TRPC3 WT mice, but not in KO mice. The present study directly demonstrated that the TRPC3 channel is involved in agonist-induced vasoconstriction and plays important role in NO-mediated vasorelaxation of intact mesenteric arteries.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Public Library of Science
dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
TRPC3
dc.subject
mesenteric arteries.
dc.subject.classification
Bioquímica y Biología Molecular
dc.subject.classification
Ciencias Biológicas
dc.subject.classification
CIENCIAS NATURALES Y EXACTAS
dc.title
Transient receptor potential canonical type 3 channels control the vascular contractility of mouse mesenteric arteries
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2019-10-28T18:26:52Z
dc.journal.volume
9
dc.journal.number
10
dc.journal.pagination
1-9
dc.journal.pais
Estados Unidos
dc.journal.ciudad
San Francisco
dc.description.fil
Fil: Yeon, Soo-In. Yonsei University College of Medicine; Corea del Sur
dc.description.fil
Fil: Kim, Joo Young. Yonsei University College Of Medicine; . Yonsei University College of Medicine; Corea del Sur
dc.description.fil
Fil: Yeon, Dong-Soo. Kwandong University College of Medicine; Corea del Sur
dc.description.fil
Fil: Abramowitz, Joel. National Institute of Environmental Health Sciences; Estados Unidos
dc.description.fil
Fil: Birnbaumer, Lutz. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. National Institute of Environmental Health Sciences; Estados Unidos
dc.description.fil
Fil: Muallem, Shmuel. National Institutes of Health; Estados Unidos
dc.description.fil
Fil: Lee, Young-Ho. Yonsei University College of Medicine; Corea del Sur
dc.journal.title
Plos One
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0110413
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1371/journal.pone.0110413
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