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Article: A dominant interference collagen X mutation disrupts hypertrophic chondrocyte pericellular matrix and glycosaminoglycan and proteoglycan distribution in transgenic mice

TitleA dominant interference collagen X mutation disrupts hypertrophic chondrocyte pericellular matrix and glycosaminoglycan and proteoglycan distribution in transgenic mice
Authors
Issue Date2001
PublisherAmerican Society for Investigative Pathology. The Journal's web site is located at http://www.amjpathol.org
Citation
American Journal Of Pathology, 2001, v. 159 n. 6, p. 2257-2269 How to Cite?
AbstractCollagen X transgenic (Tg) mice displayed skeletohematopoietic defects in tissues derived by endochondral skeletogenesis. Here we demonstrate that co-expression of the transgene product containing truncated chicken collagen X with full-length mouse collagen X in a cell-free translation system yielded chicken-mouse hybrid trimers and truncated chicken homotrimers; this indicated that the mutant could assemble with endogenous collagen X and thus had potential for dominant interference. Moreover, species-specific collagen X antibodies co-localized the transgene product with endogenous collagen X to hypertrophic cartilage in growth plates and ossification centers; proliferative chondrocytes also stained diffusely. Electron microscopy revealed a disrupted hexagonal lattice network in the hypertrophic chondrocyte pericellular matrix in Tg growth plates, as well as altered mineral deposition. Ruthenium hexamine trichloride-positive aggregates, likely glycosaminoglycans (GAGs)/proteoglycans (PGs), were also dispersed throughout the chondro-osseous junction. These defects likely resulted from transgene co-localization and dominant interference with endogenous collagen X. Moreover, altered GAG/PG distribution in growth plates of both collagen X Tg and null mice was confirmed by a paucity of staining for hyaluronan and heparan sulfate PG. A provocative hypothesis links the disruption of the collagen X pericellular network and GAG/PG decompartmentalization to the potential locus for hematopoietic failure in the collagen X mice.
Persistent Identifierhttp://hdl.handle.net/10722/48978
ISSN
2015 Impact Factor: 4.206
2015 SCImago Journal Rankings: 2.653
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorJacenko, Oen_HK
dc.contributor.authorChan, Den_HK
dc.contributor.authorFranklin, Aen_HK
dc.contributor.authorIto, Sen_HK
dc.contributor.authorUnderhill, CBen_HK
dc.contributor.authorBateman, JFen_HK
dc.contributor.authorCampbell, MRen_HK
dc.date.accessioned2008-06-12T06:31:14Z-
dc.date.available2008-06-12T06:31:14Z-
dc.date.issued2001en_HK
dc.identifier.citationAmerican Journal Of Pathology, 2001, v. 159 n. 6, p. 2257-2269en_HK
dc.identifier.issn0002-9440en_HK
dc.identifier.urihttp://hdl.handle.net/10722/48978-
dc.description.abstractCollagen X transgenic (Tg) mice displayed skeletohematopoietic defects in tissues derived by endochondral skeletogenesis. Here we demonstrate that co-expression of the transgene product containing truncated chicken collagen X with full-length mouse collagen X in a cell-free translation system yielded chicken-mouse hybrid trimers and truncated chicken homotrimers; this indicated that the mutant could assemble with endogenous collagen X and thus had potential for dominant interference. Moreover, species-specific collagen X antibodies co-localized the transgene product with endogenous collagen X to hypertrophic cartilage in growth plates and ossification centers; proliferative chondrocytes also stained diffusely. Electron microscopy revealed a disrupted hexagonal lattice network in the hypertrophic chondrocyte pericellular matrix in Tg growth plates, as well as altered mineral deposition. Ruthenium hexamine trichloride-positive aggregates, likely glycosaminoglycans (GAGs)/proteoglycans (PGs), were also dispersed throughout the chondro-osseous junction. These defects likely resulted from transgene co-localization and dominant interference with endogenous collagen X. Moreover, altered GAG/PG distribution in growth plates of both collagen X Tg and null mice was confirmed by a paucity of staining for hyaluronan and heparan sulfate PG. A provocative hypothesis links the disruption of the collagen X pericellular network and GAG/PG decompartmentalization to the potential locus for hematopoietic failure in the collagen X mice.en_HK
dc.format.extent388 bytes-
dc.format.mimetypetext/html-
dc.languageengen_HK
dc.publisherAmerican Society for Investigative Pathology. The Journal's web site is located at http://www.amjpathol.orgen_HK
dc.relation.ispartofAmerican Journal of Pathologyen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subject.meshChondrocytes - metabolismen_HK
dc.subject.meshCollagen Type X - genetics - immunology - physiologyen_HK
dc.subject.meshExtracellular Matrix - metabolismen_HK
dc.subject.meshGlycosaminoglycans - metabolismen_HK
dc.subject.meshProteoglycans - metabolismen_HK
dc.titleA dominant interference collagen X mutation disrupts hypertrophic chondrocyte pericellular matrix and glycosaminoglycan and proteoglycan distribution in transgenic miceen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0002-9440&volume=159&issue=6&spage=2257&epage=2269&date=2001&atitle=A+dominant+interference+collagen+X+mutation+disrupts+hypertrophic+chondrocyte+pericellular+matrix+and+glycosmaminoglycan+and+proteoglycan+distribution+in+transgenic+miceen_HK
dc.identifier.emailChan, D:chand@hkucc.hku.hken_HK
dc.identifier.authorityChan, D=rp00540en_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.pmid11733375-
dc.identifier.pmcidPMC1850580en_HK
dc.identifier.scopuseid_2-s2.0-0035185375en_HK
dc.identifier.hkuros68639-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0035185375&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume159en_HK
dc.identifier.issue6en_HK
dc.identifier.spage2257en_HK
dc.identifier.epage2269en_HK
dc.identifier.isiWOS:000172457400030-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridJacenko, O=7003397201en_HK
dc.identifier.scopusauthoridChan, D=7402216545en_HK
dc.identifier.scopusauthoridFranklin, A=36857237300en_HK
dc.identifier.scopusauthoridIto, S=7404826212en_HK
dc.identifier.scopusauthoridUnderhill, CB=7006074881en_HK
dc.identifier.scopusauthoridBateman, JF=16135557700en_HK
dc.identifier.scopusauthoridCampbell, MR=8079175000en_HK

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