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Hypotonic stress induces RANKL via transient receptor potential melastatin 3 (TRPM3) and vaniloid 4 (TRPV4) in human PDL cells

DC FieldValueLanguage
dc.contributor.author박원서-
dc.contributor.author손가연-
dc.contributor.author신동민-
dc.contributor.author장인익-
dc.date.accessioned2016-02-04T11:00:30Z-
dc.date.available2016-02-04T11:00:30Z-
dc.date.issued2015-
dc.identifier.issn0022-0345-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/139461-
dc.description.abstractBone remodeling occurs in response to various types of mechanical stress. The periodontal ligament (PDL) plays an important role in mechanical stress-mediated alveolar bone remodeling. However, the underlying mechanism at the cellular level has not been extensively studied. In this study, we investigated the effect of shear stress on the expression of bone remodeling factors, including receptor activator of nuclear factor-kappa B (NF-κB) ligand (RANKL) and osteoprotegerin (OPG), as well as its upstream signaling pathway in primary human PDL cells. We applied hypotonic stress to reproduce shear stress to PDL cells. Hypotonic stress induced the messenger RNA (mRNA) and protein expression of RANKL but not OPG. It also increased intracellular Ca(2+) concentration ([Ca(2+)]i). Extracellular Ca(2+) depletion and nonspecific plasma membrane Ca(2+) channel blockers completely inhibited the increase in both [Ca(2+)]i and RANKL mRNA expression. We identified the expression and activation of transient receptor potential melastatin 3 (TRPM3) and vaniloid 4 (TRPV4) channels in PDL cells. Pregnenolone sulfate (PS) and 4α-phorbol 12, 13-didecanoate (4α-PDD), which are agonists of TRPM3 and TRPV4, augmented Ca(2+) influx and RANKL mRNA expression. Both pharmacological (2-aminoethoxydiphenyl borate [2-APB], ruthenium red [RR], ononetin [Ono], and HC 067047 [HC]) and genetic (small interfering RNA [siRNA]) inhibitors of TRPM3 and TRPV4 reduced the hypotonic stress-mediated increase in [Ca(2+)]i and RANKL mRNA expression. Our study shows that hypotonic stress induced RANKL mRNA expression via TRPM3- and TRPV4-mediated extracellular Ca(2+) influx and RANKL expression. This signaling pathway in PDL cells may play a critical role in mechanical stress-mediated alveolar bone remodeling.-
dc.description.statementOfResponsibilityopen-
dc.format.extent473~481-
dc.relation.isPartOfJOURNAL OF DENTAL RESEARCH-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHBiomechanical Phenomena-
dc.subject.MESHBone Remodeling/physiology-
dc.subject.MESHBoron Compounds/pharmacology-
dc.subject.MESHCalcium Channel Blockers/pharmacology-
dc.subject.MESHCalcium Signaling/drug effects-
dc.subject.MESHCalcium Signaling/physiology-
dc.subject.MESHCell Culture Techniques-
dc.subject.MESHCells, Cultured-
dc.subject.MESHGene Silencing-
dc.subject.MESHHumans-
dc.subject.MESHHypotonic Solutions-
dc.subject.MESHMorpholines/pharmacology-
dc.subject.MESHOsteoprotegerin/biosynthesis-
dc.subject.MESHPeriodontal Ligament/cytology-
dc.subject.MESHPeriodontal Ligament/metabolism*-
dc.subject.MESHPhorbols/pharmacology-
dc.subject.MESHPregnenolone/pharmacology-
dc.subject.MESHPyrroles/pharmacology-
dc.subject.MESHRANK Ligand/antagonists & inhibitors-
dc.subject.MESHRANK Ligand/biosynthesis*-
dc.subject.MESHRNA, Messenger/metabolism-
dc.subject.MESHRNA, Small Interfering/administration & dosage-
dc.subject.MESHRuthenium Red/pharmacology-
dc.subject.MESHSignal Transduction/physiology-
dc.subject.MESHStress, Mechanical-
dc.subject.MESHTRPM Cation Channels/agonists-
dc.subject.MESHTRPM Cation Channels/antagonists & inhibitors-
dc.subject.MESHTRPM Cation Channels/physiology*-
dc.subject.MESHTRPV Cation Channels/agonists-
dc.subject.MESHTRPV Cation Channels/antagonists & inhibitors-
dc.subject.MESHTRPV Cation Channels/physiology*-
dc.titleHypotonic stress induces RANKL via transient receptor potential melastatin 3 (TRPM3) and vaniloid 4 (TRPV4) in human PDL cells-
dc.typeArticle-
dc.contributor.collegeCollege of Dentistry (치과대학)-
dc.contributor.departmentDept. of Oral Biology (구강생물학)-
dc.contributor.googleauthorG.Y. Son-
dc.contributor.googleauthorY.M. Yang-
dc.contributor.googleauthorW.S. Park-
dc.contributor.googleauthorI. Chang-
dc.contributor.googleauthorD.M. Shin-
dc.identifier.doi10.1177/0022034514567196-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA01589-
dc.contributor.localIdA01962-
dc.contributor.localIdA02091-
dc.contributor.localIdA03461-
dc.relation.journalcodeJ01367-
dc.identifier.eissn1544-0591-
dc.identifier.pmid25595364-
dc.identifier.urlhttp://jdr.sagepub.com/content/94/3/473.abstract-
dc.subject.keywordbone remodeling/regeneration-
dc.subject.keywordcell signaling-
dc.subject.keywordion channels-
dc.subject.keywordmechanotransduction-
dc.subject.keywordosmotic stress-
dc.subject.keywordperiodontal ligament-
dc.contributor.alternativeNamePark, Wonse-
dc.contributor.alternativeNameSon, Ga Yeon-
dc.contributor.alternativeNameShin, Dong Min-
dc.contributor.alternativeNameChang, In Ik-
dc.contributor.affiliatedAuthorPark, Wonse-
dc.contributor.affiliatedAuthorSon, Ga Yeon-
dc.contributor.affiliatedAuthorShin, Dong Min-
dc.contributor.affiliatedAuthorChang, In Ik-
dc.rights.accessRightsnot free-
dc.citation.volume94-
dc.citation.number3-
dc.citation.startPage473-
dc.citation.endPage481-
dc.identifier.bibliographicCitationJOURNAL OF DENTAL RESEARCH, Vol.94(3) : 473-481, 2015-
Appears in Collections:
2. College of Dentistry (치과대학) > Dept. of Oral Biology (구강생물학교실) > 1. Journal Papers
2. College of Dentistry (치과대학) > Dept. of Advanced General Dentistry (통합치의학과) > 1. Journal Papers

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