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Article: Injury-induced sequential transformation of notochordal nucleus pulposus to chondrogenic and fibrocartilaginous phenotype in the mouse

TitleInjury-induced sequential transformation of notochordal nucleus pulposus to chondrogenic and fibrocartilaginous phenotype in the mouse
Authors
KeywordsAnimal model
Degenerative disc disease
Intervertebral disc
Nucleus pulposus
Issue Date2009
PublisherJohn Wiley & Sons. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/1130
Citation
Journal Of Pathology, 2009, v. 218 n. 1, p. 113-121 How to Cite?
AbstractIntervertebral disc degeneration has been widely studied in different animal models. To test the hypothesis that needle puncture could induce progressive biochemical and molecular changes in murine discs, we established a mouse tail model to investigate the pathogenesis and molecular mechanism of puncture-induced disc degeneration. Caudal discs in mouse tails were punctured using a 31G gauge needle at controlled depth under microscopic guidance. The progress of the disc degeneration was evaluated by radiographic analysis of disc height, histological grading and glycosaminoglycan (GAG) quantification pre-operation and 1, 2, 6 and 12 weeks post-puncture. Gene and protein expression of the extracellular matrix (ECM) was analysed by RT-PCR, in situ hybridization and immunohistochemistry. Histological study and disc height analysis revealed progressive degenerative changes in the punctured discs. Compared with the pre-operation control group, total GAG content decreased 40% (p 0.05) and aggrecan (Acan), decorin (Dcn)and versican (Vcan; Cspg2) expression was down-regulated at 12 weeks post-puncture. A transient increase of Col2a1- expressing cells and elevation of collagen II protein in the nucleus pulposus (NP) was detected. Fibronectin (Fn1) expression was up-regulated 50% and deposition of collagen I in NP was observed at 12 weeks post-puncture. This study is the first to use an injury- induced model to study disc degeneration in mouse. The disc degeneration involves a transient transformation of NP from notochordal to chondrogenic and eventually into fibrocartilaginous phenotype. The degenerative changes have some similarity to human disc degeneration, suggesting that this model may potentially be used in future to study the molecular mechanism and dissect the pathways of disc degeneration. © 2009 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/58300
ISSN
2015 Impact Factor: 7.381
2015 SCImago Journal Rankings: 4.176
ISI Accession Number ID
Funding AgencyGrant Number
University of Hong Kong
Funding Information:

This work was supported by a CRCG grant from the University of Hong Kong

References

 

DC FieldValueLanguage
dc.contributor.authorYang, Fen_HK
dc.contributor.authorLeung, VYLen_HK
dc.contributor.authorLuk, KDKen_HK
dc.contributor.authorChan, Den_HK
dc.contributor.authorCheung, KMCen_HK
dc.date.accessioned2010-05-31T03:27:42Z-
dc.date.available2010-05-31T03:27:42Z-
dc.date.issued2009en_HK
dc.identifier.citationJournal Of Pathology, 2009, v. 218 n. 1, p. 113-121en_HK
dc.identifier.issn0022-3417en_HK
dc.identifier.urihttp://hdl.handle.net/10722/58300-
dc.description.abstractIntervertebral disc degeneration has been widely studied in different animal models. To test the hypothesis that needle puncture could induce progressive biochemical and molecular changes in murine discs, we established a mouse tail model to investigate the pathogenesis and molecular mechanism of puncture-induced disc degeneration. Caudal discs in mouse tails were punctured using a 31G gauge needle at controlled depth under microscopic guidance. The progress of the disc degeneration was evaluated by radiographic analysis of disc height, histological grading and glycosaminoglycan (GAG) quantification pre-operation and 1, 2, 6 and 12 weeks post-puncture. Gene and protein expression of the extracellular matrix (ECM) was analysed by RT-PCR, in situ hybridization and immunohistochemistry. Histological study and disc height analysis revealed progressive degenerative changes in the punctured discs. Compared with the pre-operation control group, total GAG content decreased 40% (p </bi>0.05) and aggrecan (Acan), decorin (Dcn)and versican (Vcan; Cspg2) expression was down-regulated at 12 weeks post-puncture. A transient increase of Col2a1- expressing cells and elevation of collagen II protein in the nucleus pulposus (NP) was detected. Fibronectin (Fn1) expression was up-regulated 50% and deposition of collagen I in NP was observed at 12 weeks post-puncture. This study is the first to use an injury- induced model to study disc degeneration in mouse. The disc degeneration involves a transient transformation of NP from notochordal to chondrogenic and eventually into fibrocartilaginous phenotype. The degenerative changes have some similarity to human disc degeneration, suggesting that this model may potentially be used in future to study the molecular mechanism and dissect the pathways of disc degeneration. © 2009 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.en_HK
dc.languageengen_HK
dc.publisherJohn Wiley & Sons. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/1130en_HK
dc.relation.ispartofJournal of Pathologyen_HK
dc.rightsJournal of Pathology. Copyright © John Wiley & Sons Ltd.en_HK
dc.subjectAnimal modelen_HK
dc.subjectDegenerative disc diseaseen_HK
dc.subjectIntervertebral discen_HK
dc.subjectNucleus pulposusen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshCartilage - metabolism - pathologyen_HK
dc.subject.meshCollagen Type II - metabolismen_HK
dc.subject.meshDisease Models, Animalen_HK
dc.subject.meshExtracellular Matrix Proteins - analysis - geneticsen_HK
dc.subject.meshFibrocartilage - metabolism - pathologyen_HK
dc.subject.meshGene Expressionen_HK
dc.subject.meshGlycosaminoglycans - metabolismen_HK
dc.subject.meshImmunohistochemistryen_HK
dc.subject.meshIn Situ Hybridizationen_HK
dc.subject.meshIntervertebral Disc - injuries - metabolism - pathologyen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Mutant Strainsen_HK
dc.subject.meshNotochord - metabolism - pathologyen_HK
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_HK
dc.subject.meshSpinal Diseases - metabolism - pathologyen_HK
dc.subject.meshTailen_HK
dc.subject.meshTime Factorsen_HK
dc.titleInjury-induced sequential transformation of notochordal nucleus pulposus to chondrogenic and fibrocartilaginous phenotype in the mouseen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-3417&volume=218&issue=1&spage=113&epage=21&date=2009&atitle=Injury-induced+sequential+transformation+of+notochordal+nucleus+pulposus+to+chondrogenic+and+fibrocartilaginous+phenotype+in+the+mouseen_HK
dc.identifier.emailLeung, VYL: vicleung@hku.hken_HK
dc.identifier.emailLuk, KDK: hcm21000@hku.hken_HK
dc.identifier.emailChan, D: chand@hkucc.hku.hken_HK
dc.identifier.emailCheung, KMC: cheungmc@hku.hken_HK
dc.identifier.authorityLeung, VYL=rp01764en_HK
dc.identifier.authorityLuk, KDK=rp00333en_HK
dc.identifier.authorityChan, D=rp00540en_HK
dc.identifier.authorityCheung, KMC=rp00387en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/path.2519en_HK
dc.identifier.pmid19288580-
dc.identifier.scopuseid_2-s2.0-66749147825en_HK
dc.identifier.hkuros160663en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-66749147825&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume218en_HK
dc.identifier.issue1en_HK
dc.identifier.spage113en_HK
dc.identifier.epage121en_HK
dc.identifier.isiWOS:000265546200012-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridYang, F=35354574000en_HK
dc.identifier.scopusauthoridLeung, VYL=35337438900en_HK
dc.identifier.scopusauthoridLuk, KDK=7201921573en_HK
dc.identifier.scopusauthoridChan, D=7402216545en_HK
dc.identifier.scopusauthoridCheung, KMC=7402406754en_HK

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