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Opposite regulatory effects of TRPC1 and TRPC5 on neurite outgrowth in PC12 cells.

DC FieldValueLanguage
dc.contributor.author김주영-
dc.contributor.author박현우-
dc.contributor.author이민구-
dc.contributor.author정우영-
dc.date.accessioned2014-12-19T16:38:45Z-
dc.date.available2014-12-19T16:38:45Z-
dc.date.issued2012-
dc.identifier.issn0898-6568-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/89921-
dc.description.abstractThe transient receptor potential (TRPC) family of Ca²⁺ permeable, non-selective cation channels is abundantly expressed in the brain, and can function as store-operated (SOC) and store-independent channels depending on their interaction with the ER Ca²⁺ sensor STIM1. TRPC1 and TRPC5 have critical roles in neurite outgrowth, however which of their functions regulate neurite outgrowth is unknown. In this study, we investigated the effects of TRPC channels and their STIM1-induced SOC activity on neurite outgrowth of PC12 cells. We report that PC12 cell differentiation down-regulates TRPC5 expression, whereas TRPC1 expression is retained. TRPC1 and TRPC5 interact with STIM1 through the STIM1 ERM domain. Transfection of TRPC1 and TRPC5 increased the receptor-activated Ca²⁺ influx that was markedly augmented by the co-expression of STIM1. Topical expression of TRPC1 in PC12 cells markedly increased neurite outgrowth while that of TRPC5 suppressed neurite outgrowth. Suppression of neurite outgrowth by TRPC5 requires the channel function of TRPC5. However, strikingly, multiple lines of evidence show that the TRPC1-induced neurite outgrowth was independent of TRPC1-mediated Ca²⁺ influx. Thus, a) TRPC1 and TRPC5 similarly increased Ca²⁺ influx but only TRPC1 induced neurite outgrowth, b) the constitutively STIM1(D76A) mutant that activates Ca²⁺ influx by TRPC and Orai channels did not increase neurite outgrowth, c) co-expression of TRPC5 with TRPC1 suppressed the effect of TRPC1 on neurite outgrowth, d) and most notable, channel-dead pore mutant of TRPC1 increased neurite outgrowth to the same extent as TRPC1(WT). Suppression of TRPC1-induced neurite outgrowth by TRPC5 was due to a marked reduction in the surface expression of TRPC1. We conclude that the regulation of neurite outgrowth by TRPC1 is independent of Ca²⁺ influx and TRPC1-promoted neurite outgrowth depends on the surface expression of TRPC1. It is likely that TRPC1 acts as a scaffold at the cell surface to assemble a signaling complex to stimulate neurite outgrowth.-
dc.description.statementOfResponsibilityopen-
dc.relation.isPartOfCELLULAR SIGNALLING-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAnimals-
dc.subject.MESHCalcium/metabolism*-
dc.subject.MESHCalcium Channels/genetics-
dc.subject.MESHCalcium Channels/metabolism-
dc.subject.MESHCell Differentiation-
dc.subject.MESHCell Membrane/genetics-
dc.subject.MESHCell Membrane/metabolism-
dc.subject.MESHCell Proliferation-
dc.subject.MESHGene Expression Regulation-
dc.subject.MESHHEK293 Cells-
dc.subject.MESHHeLa Cells-
dc.subject.MESHHumans-
dc.subject.MESHIon Channel Gating-
dc.subject.MESHMembrane Glycoproteins/genetics-
dc.subject.MESHMembrane Glycoproteins/metabolism-
dc.subject.MESHNeurites/physiology*-
dc.subject.MESHNeurogenesis-
dc.subject.MESHPC12 Cells-
dc.subject.MESHProtein Structure, Tertiary-
dc.subject.MESHRats-
dc.subject.MESHSignal Transduction/genetics*-
dc.subject.MESHStromal Interaction Molecule 1-
dc.subject.MESHTRPC Cation Channels/genetics*-
dc.subject.MESHTRPC Cation Channels/metabolism-
dc.subject.MESHTransfection-
dc.titleOpposite regulatory effects of TRPC1 and TRPC5 on neurite outgrowth in PC12 cells.-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Pharmacology (약리학)-
dc.contributor.googleauthorDae Keon Heo-
dc.contributor.googleauthorWoo Young Chung-
dc.contributor.googleauthorHyun Woo Park-
dc.contributor.googleauthorJoseph P. Yuan-
dc.contributor.googleauthorMin Goo Lee-
dc.contributor.googleauthorJoo Young Kim-
dc.identifier.doi22201561-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00942-
dc.contributor.localIdA01743-
dc.contributor.localIdA02781-
dc.contributor.localIdA03668-
dc.relation.journalcodeJ00502-
dc.identifier.eissn1873-3913-
dc.identifier.pmid22201561-
dc.identifier.urlhttp://www.sciencedirect.com/science/article/pii/S0898656811003895-
dc.subject.keywordTRPC channels-
dc.subject.keywordSTIM1-
dc.subject.keywordSOC-
dc.subject.keywordCalcium influx-
dc.subject.keywordNeurite outgrowth-
dc.subject.keywordSurface expression-
dc.contributor.alternativeNameKim, Joo Young-
dc.contributor.alternativeNamePark, Hyun Woo-
dc.contributor.alternativeNameLee, Min Goo-
dc.contributor.alternativeNameChung, Woo Young-
dc.contributor.affiliatedAuthorKim, Joo Young-
dc.contributor.affiliatedAuthorPark, Hyun Woo-
dc.contributor.affiliatedAuthorLee, Min Goo-
dc.contributor.affiliatedAuthorChung, Woo Young-
dc.citation.volume24-
dc.citation.number4-
dc.citation.startPage899-
dc.citation.endPage906-
dc.identifier.bibliographicCitationCELLULAR SIGNALLING, Vol.24(4) : 899-906, 2012-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Pharmacology (약리학교실) > 1. Journal Papers

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