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Article: Abnormal compartmentalization of cartilage matrix components in mice lacking collagen X: Implications for function

TitleAbnormal compartmentalization of cartilage matrix components in mice lacking collagen X: Implications for function
Authors
Issue Date1997
PublisherRockefeller University Press. The Journal's web site is located at http://www.jcb.org
Citation
Journal Of Cell Biology, 1997, v. 136 n. 2, p. 459-471 How to Cite?
AbstractThere are conflicting views on whether collagen X is a purely structural molecule, or regulates bone mineralization during endochondral ossification. Mutations is the human collagen α1(X) gene (COL10A1) in Schmid metaphyseal chondrodysplasia (SMCD) suggest a supportive role. But mouse collagen α1(X) gene (Col10A1) null mutants were previously reported to show no obvious phenotypic change. We have generated collagen X deficient mice, which shows that deficiency does have phenotypic consequences which partly resemble SMCD, such as abnormal trabecular bone architecture. In particular, the mutant mice develop coxa vara, a phenotypic change common in human SMCD. Other consequences of the mutation are reduction in thickness of growth plate resting zone and articular cartilage, altered bone content, and atypical distribution of matrix components within growth plate cartilage. We propose that collagen X plays a role in the normal distribution of matrix vesicles and proteoglycans within the growth plate matrix. Collagen X deficiency impacts on the supporting properties of the growth plate and the mineralization process, resulting in abnormal trabecular bone. This hypothesis would accommodate the previously conflicting views of the function of collagen X and of the molecular pathogenesis of SMCD.
Persistent Identifierhttp://hdl.handle.net/10722/53318
ISSN
2015 Impact Factor: 8.717
2015 SCImago Journal Rankings: 7.923
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorKwan, KMen_HK
dc.contributor.authorPang, MKMen_HK
dc.contributor.authorZhou, Sen_HK
dc.contributor.authorCowan, SKen_HK
dc.contributor.authorKong, RYCen_HK
dc.contributor.authorPfordte, Ten_HK
dc.contributor.authorOlsen, BRen_HK
dc.contributor.authorSillence, DOen_HK
dc.contributor.authorTam, PPLen_HK
dc.contributor.authorCheah, KSEen_HK
dc.date.accessioned2009-04-03T07:12:14Z-
dc.date.available2009-04-03T07:12:14Z-
dc.date.issued1997en_HK
dc.identifier.citationJournal Of Cell Biology, 1997, v. 136 n. 2, p. 459-471en_HK
dc.identifier.issn0021-9525en_HK
dc.identifier.urihttp://hdl.handle.net/10722/53318-
dc.description.abstractThere are conflicting views on whether collagen X is a purely structural molecule, or regulates bone mineralization during endochondral ossification. Mutations is the human collagen α1(X) gene (COL10A1) in Schmid metaphyseal chondrodysplasia (SMCD) suggest a supportive role. But mouse collagen α1(X) gene (Col10A1) null mutants were previously reported to show no obvious phenotypic change. We have generated collagen X deficient mice, which shows that deficiency does have phenotypic consequences which partly resemble SMCD, such as abnormal trabecular bone architecture. In particular, the mutant mice develop coxa vara, a phenotypic change common in human SMCD. Other consequences of the mutation are reduction in thickness of growth plate resting zone and articular cartilage, altered bone content, and atypical distribution of matrix components within growth plate cartilage. We propose that collagen X plays a role in the normal distribution of matrix vesicles and proteoglycans within the growth plate matrix. Collagen X deficiency impacts on the supporting properties of the growth plate and the mineralization process, resulting in abnormal trabecular bone. This hypothesis would accommodate the previously conflicting views of the function of collagen X and of the molecular pathogenesis of SMCD.en_HK
dc.languageengen_HK
dc.publisherRockefeller University Press. The Journal's web site is located at http://www.jcb.orgen_HK
dc.relation.ispartofJournal of Cell Biologyen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.rightsThe Journal of Cell Biology. Copyright © Rockefeller University Press.en_HK
dc.subject.meshCollagen - deficiency - genetics - physiologyen_HK
dc.subject.meshGrowth Plate - chemistry - cytologyen_HK
dc.subject.meshOsteogenesisen_HK
dc.subject.meshProteoglycans - analysisen_HK
dc.subject.meshCartilage, Articular - chemistry - cytologyen_HK
dc.titleAbnormal compartmentalization of cartilage matrix components in mice lacking collagen X: Implications for functionen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0021-9525&volume=136&issue=2&spage=459&epage=471&date=1997&atitle=Abnormal+compartmentalization+of+cartilage+matrix+components+in+mice+lacking+collagen+X:+implications+for+functionen_HK
dc.identifier.emailCheah, KSE:hrmbdkc@hku.hken_HK
dc.identifier.authorityCheah, KSE=rp00342en_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.doi10.1083/jcb.136.2.459en_HK
dc.identifier.pmid9015315-
dc.identifier.pmcidPMC2134813-
dc.identifier.scopuseid_2-s2.0-0010098815en_HK
dc.identifier.hkuros25351-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0010098815&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume136en_HK
dc.identifier.issue2en_HK
dc.identifier.spage459en_HK
dc.identifier.epage471en_HK
dc.identifier.isiWOS:A1997WF46600020-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridKwan, KM=7006405800en_HK
dc.identifier.scopusauthoridPang, MKM=7102068634en_HK
dc.identifier.scopusauthoridZhou, S=7404166224en_HK
dc.identifier.scopusauthoridCowan, SK=7004660335en_HK
dc.identifier.scopusauthoridKong, RYC=7005290687en_HK
dc.identifier.scopusauthoridPfordte, T=6504348541en_HK
dc.identifier.scopusauthoridOlsen, BR=35403161200en_HK
dc.identifier.scopusauthoridSillence, DO=7006527427en_HK
dc.identifier.scopusauthoridTam, PPL=7202539412en_HK
dc.identifier.scopusauthoridCheah, KSE=35387746200en_HK

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