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• W2949273764 endingPage "20170335" @default.
• W2949273764 startingPage "20170335" @default.
• W2949273764 abstract "Collagen is the major structural component of cartilage, and mutations in the genes encoding type XI collagen are associated with severe skeletal dysplasias (fibrochondrogenesis and Stickler syndrome) and early-onset osteoarthritis (OA). The impact of the lack of type XI collagen on cell behaviour and mechanical performance during skeleton development is unknown. We studied a zebrafish mutant for col11a2 and evaluated cartilage, bone development and mechanical properties to address this. We show that in col11a2 mutants, type II collagen is made but is prematurely degraded in maturing cartilage and ectopically expressed in the joint. These changes are correlated with increased stiffness of both bone and cartilage; quantified using atomic force microscopy. In the mutants, the skeletal rudiment terminal region in the jaw joint is broader and the interzone smaller. These differences in shape and material properties impact on joint function and mechanical performance, which we modelled using finite element analyses. Finally, we show that col11a2 heterozygous carriers reach adulthood but show signs of severe early-onset OA. Taken together, our data demonstrate a key role for type XI collagen in maintaining the properties of cartilage matrix; which when lost leads to alterations to cell behaviour that give rise to joint pathologies. This article is part of the Theo Murphy meeting issue ‘Mechanics of development’." @default.
• W2949273764 created "2019-06-27" @default.
• W2949273764 creator A5007984802 @default.
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• W2949273764 creator A5051114666 @default.
• W2949273764 creator A5088961033 @default.
• W2949273764 date "2018-09-24" @default.
• W2949273764 modified "2023-10-01" @default.
• W2949273764 title "The mechanical impact of <i>col11a2</i> loss on joints; <i>col11a2</i> mutant zebrafish show changes to joint development and function, which leads to early-onset osteoarthritis" @default.
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• W2949273764 doi "https://doi.org/10.1098/rstb.2017.0335" @default.
• W2949273764 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6158203" @default.
• W2949273764 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30249781" @default.
• W2949273764 hasPublicationYear "2018" @default.
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