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Targeting of focal adhesion kinase by small interfering RNAs reduces chondrocyte redifferentiation capacity in alginate beads culture with type II collagen

DC Field Value Language
dc.contributor.author이진우-
dc.date.accessioned2015-04-24T16:24:01Z-
dc.date.available2015-04-24T16:24:01Z-
dc.date.issued2009-
dc.identifier.issn0021-9541-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/103443-
dc.description.abstractType II collagen is a major protein that maintains biological and mechanical characteristics in articular cartilage. Focal adhesion kinase (FAK) is known to play a central role in integrin signaling of cell-extracellular matrix (ECM) interactions, and chondrocyte-type II collagen interactions are very important for cartilage homeostasis. In this study, we focused on phosphorylation of FAK and MAP kinase in chondrocyte-type II collagen interaction and dedifferentiation, and the effects of FAK knockdown on chondrocyte-specific gene expression and cell proliferation were determined. The addition of exogenous type II collagen to chondrocytes increased levels of tyrosine phosphorylation, p-FAK(Y397), and p-ERK1/2. In contrast, expression levels of p-FAK(Y397) and p-ERK1/2, but not p-Smad2/3, were decreased in dedifferentiated chondrocytes with loss of type II collagen expression. Type II collagen expression was significantly increased when dedifferentiated chondrocytes were transferred to alginate beads with TGF-beta1 or type II collagen, but transfected cells with small interfering RNA for FAK (FAK-siRNA) inhibited mRNA expression of type II collagen and SOX-6 compared to the control. These FAK-siRNA-transfected cells could not recover type II collagen even in the presence of TGF-beta1 or type II collagen in alginate beads culture. We also found that FAK-siRNA-transfected cells decreased cell proliferation rate, but there was no effect on glycosaminoglycans (GAGs) secretion. We suggest that FAK is essentially required in chondrocyte communication with type II collagen by regulating type II collagen expression and cell proliferation.-
dc.description.statementOfResponsibilityopen-
dc.format.extent623~630-
dc.relation.isPartOfJOURNAL OF CELLULAR PHYSIOLOGY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAdult-
dc.subject.MESHAlginates/metabolism*-
dc.subject.MESHAnimals-
dc.subject.MESHCell Culture Techniques-
dc.subject.MESHCell Dedifferentiation-
dc.subject.MESHCell Differentiation*-
dc.subject.MESHCell Proliferation-
dc.subject.MESHCell Shape-
dc.subject.MESHChondrocytes/cytology*-
dc.subject.MESHChondrocytes/enzymology*-
dc.subject.MESHCollagen Type II/metabolism*-
dc.subject.MESHEnzyme Activation-
dc.subject.MESHExtracellular Signal-Regulated MAP Kinases/metabolism-
dc.subject.MESHFocal Adhesion Protein-Tyrosine Kinases/metabolism*-
dc.subject.MESHGene Expression Regulation-
dc.subject.MESHGlucuronic Acid/metabolism-
dc.subject.MESHGlycosaminoglycans/metabolism-
dc.subject.MESHHexuronic Acids/metabolism-
dc.subject.MESHHumans-
dc.subject.MESHMicrospheres-
dc.subject.MESHMiddle Aged-
dc.subject.MESHPhosphorylation-
dc.subject.MESHRNA, Small Interfering/metabolism*-
dc.subject.MESHSmad Proteins/metabolism-
dc.subject.MESHSwine-
dc.titleTargeting of focal adhesion kinase by small interfering RNAs reduces chondrocyte redifferentiation capacity in alginate beads culture with type II collagen-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Orthopedic Surgery (정형외과학)-
dc.contributor.googleauthorYUN HEE KIM-
dc.contributor.googleauthorJIN WOO LEE-
dc.identifier.doi10.1002/jcp.21637-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA03230-
dc.relation.journalcodeJ01304-
dc.identifier.eissn1097-4652-
dc.identifier.pmid19006177-
dc.identifier.urlhttp://onlinelibrary.wiley.com/doi/10.1002/jcp.21637/abstract-
dc.contributor.alternativeNameLee, Jin Woo-
dc.contributor.affiliatedAuthorLee, Jin Woo-
dc.citation.volume218-
dc.citation.number3-
dc.citation.startPage623-
dc.citation.endPage630-
dc.identifier.bibliographicCitationJOURNAL OF CELLULAR PHYSIOLOGY, Vol.218(3) : 623-630, 2009-
dc.identifier.rimsid36007-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Orthopedic Surgery (정형외과학교실) > 1. Journal Papers

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