{"@context":{"@vocab":"https://cir.nii.ac.jp/schema/1.0/","rdfs":"http://www.w3.org/2000/01/rdf-schema#","dc":"http://purl.org/dc/elements/1.1/","dcterms":"http://purl.org/dc/terms/","foaf":"http://xmlns.com/foaf/0.1/","prism":"http://prismstandard.org/namespaces/basic/2.0/","cinii":"http://ci.nii.ac.jp/ns/1.0/","datacite":"https://schema.datacite.org/meta/kernel-4/","ndl":"http://ndl.go.jp/dcndl/terms/","jpcoar":"https://github.com/JPCOAR/schema/blob/master/2.0/"},"@id":"https://cir.nii.ac.jp/crid/1361699995790548736.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.1161/01.res.0000023391.40106.a8"}},{"identifier":{"@type":"URI","@value":"https://www.ahajournals.org/doi/full/10.1161/01.RES.0000023391.40106.A8"}},{"identifier":{"@type":"NAID","@value":"30022674800"}}],"dc:title":[{"@value":"Impairment of Store-Operated Ca\n            <sup>2+</sup>\n            Entry in TRPC4\n            <sup>−/−</sup>\n            Mice Interferes With Increase in Lung Microvascular Permeability"}],"description":[{"type":"abstract","notation":[{"@value":"<jats:p>\n            We investigated the possibility that the TRPC gene family of putative store-operated Ca\n            <jats:sup>2+</jats:sup>\n            entry channels contributes to the increase in microvascular endothelial permeability by prolonging the rise in intracellular Ca\n            <jats:sup>2+</jats:sup>\n            signaling. Studies were made in wild-type (wt) and TRPC4 knockout (TRPC4\n            <jats:sup>−/−</jats:sup>\n            ) mice and lung vascular endothelial cells (LECs) isolated from these animals. RT-PCR showed expression of TRPC1, TRPC3, TRPC4, and TRPC6 mRNA in wt LECs, but TRPC4 mRNA expression was not detected in TRPC4\n            <jats:sup>−/−</jats:sup>\n            LECs. We studied the response to thrombin because it is known to increase endothelial permeability by the activation of G protein-coupled proteinase-activated receptor-1 (PAR-1). In wt LECs, thrombin or PAR-1 agonist peptide (TFLLRNPNDK-NH\n            <jats:sub>2</jats:sub>\n            ) resulted in a prolonged Ca\n            <jats:sup>2+</jats:sup>\n            transient secondary to influx of Ca\n            <jats:sup>2+</jats:sup>\n            . Ca\n            <jats:sup>2+</jats:sup>\n            influx activated by thrombin was blocked by La\n            <jats:sup>3+</jats:sup>\n            (1 μmol/L). In TRPC4\n            <jats:sup>−/−</jats:sup>\n            LECs, thrombin or TFLLRNPNDK-NH\n            <jats:sub>2</jats:sub>\n            produced a similar initial increase of intracellular Ca\n            <jats:sup>2+</jats:sup>\n            secondary to Ca\n            <jats:sup>2+</jats:sup>\n            store depletion, but Ca\n            <jats:sup>2+</jats:sup>\n            influx induced by these agonists was drastically reduced. The defect in Ca\n            <jats:sup>2+</jats:sup>\n            influx in TRPC4\n            <jats:sup>−/−</jats:sup>\n            endothelial cells was associated with lack of thrombin-induced actin-stress fiber formation and a reduced endothelial cell retraction response. In isolated-perfused mouse lungs, the PAR-1 agonist peptide increased microvessel filtration coefficient (K\n            <jats:sub>f,c</jats:sub>\n            ), a measure of vascular permeability, by a factor of 2.8 in wt and 1.4 in TRPC4\n            <jats:sup>−/−</jats:sup>\n            ; La\n            <jats:sup>3+</jats:sup>\n            (1 μmol/L) addition to wt lung perfusate reduced the agonist effect to that observed in TRPC4\n            <jats:sup>−/−</jats:sup>\n            . These results show that TRPC4-dependent Ca\n            <jats:sup>2+</jats:sup>\n            entry in mouse LECs is a key determinant of increased microvascular permeability.\n          </jats:p>"}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1381699995790548736","@type":"Researcher","foaf:name":[{"@value":"Chinnaswamy Tiruppathi"}],"jpcoar:affiliationName":[{"@value":"From the Department of Pharmacology, The University of Illinois, Chicago, Ill; and Universitat des Saarlandes (M.F., V.F.), Institut fur Pharmakologie und Toxikologie, Homburg, Germany."}]},{"@id":"https://cir.nii.ac.jp/crid/1381699995790548737","@type":"Researcher","foaf:name":[{"@value":"Marc Freichel"}],"jpcoar:affiliationName":[{"@value":"From the Department of Pharmacology, The University of Illinois, Chicago, Ill; and Universitat des Saarlandes (M.F., V.F.), Institut fur Pharmakologie und Toxikologie, Homburg, Germany."}]},{"@id":"https://cir.nii.ac.jp/crid/1381699995790548741","@type":"Researcher","foaf:name":[{"@value":"Stephen M. Vogel"}],"jpcoar:affiliationName":[{"@value":"From the Department of Pharmacology, The University of Illinois, Chicago, Ill; and Universitat des Saarlandes (M.F., V.F.), Institut fur Pharmakologie und Toxikologie, Homburg, Germany."}]},{"@id":"https://cir.nii.ac.jp/crid/1381699995790548738","@type":"Researcher","foaf:name":[{"@value":"Biman C. Paria"}],"jpcoar:affiliationName":[{"@value":"From the Department of Pharmacology, The University of Illinois, Chicago, Ill; and Universitat des Saarlandes (M.F., V.F.), Institut fur Pharmakologie und Toxikologie, Homburg, Germany."}]},{"@id":"https://cir.nii.ac.jp/crid/1381699995790548739","@type":"Researcher","foaf:name":[{"@value":"Dolly Mehta"}],"jpcoar:affiliationName":[{"@value":"From the Department of Pharmacology, The University of Illinois, Chicago, Ill; and Universitat des Saarlandes (M.F., V.F.), Institut fur Pharmakologie und Toxikologie, Homburg, Germany."}]},{"@id":"https://cir.nii.ac.jp/crid/1381699995790548742","@type":"Researcher","foaf:name":[{"@value":"Veit Flockerzi"}],"jpcoar:affiliationName":[{"@value":"From the Department of Pharmacology, The University of Illinois, Chicago, Ill; and Universitat des Saarlandes (M.F., V.F.), Institut fur Pharmakologie und Toxikologie, Homburg, Germany."}]},{"@id":"https://cir.nii.ac.jp/crid/1381699995790548740","@type":"Researcher","foaf:name":[{"@value":"Asrar B. Malik"}],"jpcoar:affiliationName":[{"@value":"From the Department of Pharmacology, The University of Illinois, Chicago, Ill; and Universitat des Saarlandes (M.F., V.F.), Institut fur Pharmakologie und Toxikologie, Homburg, Germany."}]}],"publication":{"publicationIdentifier":[{"@type":"PISSN","@value":"00097330"},{"@type":"EISSN","@value":"15244571"}],"prism:publicationName":[{"@value":"Circulation Research"}],"dc:publisher":[{"@value":"Ovid Technologies (Wolters Kluwer Health)"}],"prism:publicationDate":"2002-07-12","prism:volume":"91","prism:number":"1","prism:startingPage":"70","prism:endingPage":"76"},"reviewed":"false","url":[{"@id":"https://www.ahajournals.org/doi/full/10.1161/01.RES.0000023391.40106.A8"}],"createdAt":"2002-07-28","modifiedAt":"2024-05-12","relatedProduct":[{"@id":"https://cir.nii.ac.jp/crid/1360002216061221248","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"TRPV4 partially participates in proliferation of human brain capillary endothelial cells"}]},{"@id":"https://cir.nii.ac.jp/crid/1360848662967139712","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Regulation of cardiovascular TRP channel functions along the NO–cGMP–PKG axis"}]},{"@id":"https://cir.nii.ac.jp/crid/1390001205177651584","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy","isCitedBy"],"jpcoar:relatedTitle":[{"@language":"en","@value":"Transient Receptor Potential Protein as a Novel Non-Voltage-Gated Ca2+ Entry Channel Involved in Diverse Pathophysiological Functions"},{"@value":"Transient Receptor Potential Protein as a Novel Non-Voltage-Gated Ca〔2+〕 Entry Channel Involved in Diverse Pathophysiological Functions"}]},{"@id":"https://cir.nii.ac.jp/crid/1573387450052250880","@type":"Article","relationType":["isCitedBy"],"jpcoar:relatedTitle":[{"@language":"ja","@value":"血管内皮細胞機能と新規Ca流入チャネル"},{"@language":"en","@value":"Transient receptor Potential channels in endothelial cells"}]}],"dataSourceIdentifier":[{"@type":"CROSSREF","@value":"10.1161/01.res.0000023391.40106.a8"},{"@type":"CIA","@value":"30022674800"},{"@type":"CROSSREF","@value":"10.1016/j.lfs.2013.01.002_references_DOI_WDIFq12ZRRBU0cTQVAdGwt1A03J"},{"@type":"CROSSREF","@value":"10.1586/ecp.10.15_references_DOI_WDIFq12ZRRBU0cTQVAdGwt1A03J"},{"@type":"CROSSREF","@value":"10.1254/jphs.91.271_references_DOI_WDIFq12ZRRBU0cTQVAdGwt1A03J"}]}