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- Publisher Website: 10.1002/path.2519
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- PMID: 19288580
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Article: Injury-induced sequential transformation of notochordal nucleus pulposus to chondrogenic and fibrocartilaginous phenotype in the mouse
Title | Injury-induced sequential transformation of notochordal nucleus pulposus to chondrogenic and fibrocartilaginous phenotype in the mouse | ||||
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Authors | |||||
Keywords | Animal model Degenerative disc disease Intervertebral disc Nucleus pulposus | ||||
Issue Date | 2009 | ||||
Publisher | John 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? | ||||
Abstract | Intervertebral 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 Identifier | http://hdl.handle.net/10722/58300 | ||||
ISSN | 2023 Impact Factor: 5.6 2023 SCImago Journal Rankings: 2.426 | ||||
ISI Accession Number ID |
Funding Information: This work was supported by a CRCG grant from the University of Hong Kong | ||||
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Yang, F | en_HK |
dc.contributor.author | Leung, VYL | en_HK |
dc.contributor.author | Luk, KDK | en_HK |
dc.contributor.author | Chan, D | en_HK |
dc.contributor.author | Cheung, KMC | en_HK |
dc.date.accessioned | 2010-05-31T03:27:42Z | - |
dc.date.available | 2010-05-31T03:27:42Z | - |
dc.date.issued | 2009 | en_HK |
dc.identifier.citation | Journal Of Pathology, 2009, v. 218 n. 1, p. 113-121 | en_HK |
dc.identifier.issn | 0022-3417 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/58300 | - |
dc.description.abstract | Intervertebral 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.language | eng | en_HK |
dc.publisher | John Wiley & Sons. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/1130 | en_HK |
dc.relation.ispartof | Journal of Pathology | en_HK |
dc.rights | Journal of Pathology. Copyright © John Wiley & Sons Ltd. | en_HK |
dc.subject | Animal model | en_HK |
dc.subject | Degenerative disc disease | en_HK |
dc.subject | Intervertebral disc | en_HK |
dc.subject | Nucleus pulposus | en_HK |
dc.subject.mesh | Animals | en_HK |
dc.subject.mesh | Cartilage - metabolism - pathology | en_HK |
dc.subject.mesh | Collagen Type II - metabolism | en_HK |
dc.subject.mesh | Disease Models, Animal | en_HK |
dc.subject.mesh | Extracellular Matrix Proteins - analysis - genetics | en_HK |
dc.subject.mesh | Fibrocartilage - metabolism - pathology | en_HK |
dc.subject.mesh | Gene Expression | en_HK |
dc.subject.mesh | Glycosaminoglycans - metabolism | en_HK |
dc.subject.mesh | Immunohistochemistry | en_HK |
dc.subject.mesh | In Situ Hybridization | en_HK |
dc.subject.mesh | Intervertebral Disc - injuries - metabolism - pathology | en_HK |
dc.subject.mesh | Mice | en_HK |
dc.subject.mesh | Mice, Mutant Strains | en_HK |
dc.subject.mesh | Notochord - metabolism - pathology | en_HK |
dc.subject.mesh | Reverse Transcriptase Polymerase Chain Reaction | en_HK |
dc.subject.mesh | Spinal Diseases - metabolism - pathology | en_HK |
dc.subject.mesh | Tail | en_HK |
dc.subject.mesh | Time Factors | en_HK |
dc.title | Injury-induced sequential transformation of notochordal nucleus pulposus to chondrogenic and fibrocartilaginous phenotype in the mouse | en_HK |
dc.type | Article | en_HK |
dc.identifier.openurl | http://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+mouse | en_HK |
dc.identifier.email | Leung, VYL: vicleung@hku.hk | en_HK |
dc.identifier.email | Luk, KDK: hcm21000@hku.hk | en_HK |
dc.identifier.email | Chan, D: chand@hkucc.hku.hk | en_HK |
dc.identifier.email | Cheung, KMC: cheungmc@hku.hk | en_HK |
dc.identifier.authority | Leung, VYL=rp01764 | en_HK |
dc.identifier.authority | Luk, KDK=rp00333 | en_HK |
dc.identifier.authority | Chan, D=rp00540 | en_HK |
dc.identifier.authority | Cheung, KMC=rp00387 | en_HK |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1002/path.2519 | en_HK |
dc.identifier.pmid | 19288580 | - |
dc.identifier.scopus | eid_2-s2.0-66749147825 | en_HK |
dc.identifier.hkuros | 160663 | en_HK |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-66749147825&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 218 | en_HK |
dc.identifier.issue | 1 | en_HK |
dc.identifier.spage | 113 | en_HK |
dc.identifier.epage | 121 | en_HK |
dc.identifier.isi | WOS:000265546200012 | - |
dc.publisher.place | United Kingdom | en_HK |
dc.identifier.scopusauthorid | Yang, F=35354574000 | en_HK |
dc.identifier.scopusauthorid | Leung, VYL=35337438900 | en_HK |
dc.identifier.scopusauthorid | Luk, KDK=7201921573 | en_HK |
dc.identifier.scopusauthorid | Chan, D=7402216545 | en_HK |
dc.identifier.scopusauthorid | Cheung, KMC=7402406754 | en_HK |
dc.identifier.issnl | 0022-3417 | - |