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Conference Paper: MMP14 regulates the lineage progression of hypertrophic chondrocytes
Title | MMP14 regulates the lineage progression of hypertrophic chondrocytes |
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Authors | |
Issue Date | 2013 |
Publisher | The Chinese University of Hong Kong. |
Citation | The 2013 Hong Kong Inter-University Biochemistry Postgraduate Symposium, Hong Kong, 15 June 2013. In Symposium Booklet, 2013, abstract P02 How to Cite? |
Abstract | It is traditionally believed that chondrocytes and osteoblasts are two separate lineages with hypertrophic chondrocytes (HCs) being the terminal stage of chondrocyte differentiation, culminating in apoptosis. However, we have shown that HCs can contribute to the full osteoblast (Obs) lineage in vivo. MMP14 is a transmembrane matrix metalloproteinase responsible for matrix remodeling that is highly expressed at the chondro‐osseous junction which coincides with the transition from HCs to Obs. Knockout of Mmp14 in mice results in impaired endochondral ossification. To test whether loss of MMP14 has an impact on the HC to Obs transition, we have employed a genetic recombination approach to track and compare the fate of HCs in wild‐type and Mmp14 conditional and total null mutants. Both complete and conditional deletion of MMP14 activity results in increased number of HC‐descendent cells in the trabecular bone. Surprisingly, conditional knockout of Mmp14 in HC‐descendent cells results in increased trabecular bone formation. Our results suggest that MMP14 in general negatively regulates HC to Obs transition. |
Persistent Identifier | http://hdl.handle.net/10722/189755 |
DC Field | Value | Language |
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dc.contributor.author | Chu, TL | en_US |
dc.contributor.author | Tsang, KY | en_US |
dc.contributor.author | Tsang, SW | en_US |
dc.contributor.author | Zhou, Z | en_US |
dc.contributor.author | Cheah, KSE | en_US |
dc.date.accessioned | 2013-09-17T14:56:05Z | - |
dc.date.available | 2013-09-17T14:56:05Z | - |
dc.date.issued | 2013 | - |
dc.identifier.citation | The 2013 Hong Kong Inter-University Biochemistry Postgraduate Symposium, Hong Kong, 15 June 2013. In Symposium Booklet, 2013, abstract P02 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/189755 | - |
dc.description.abstract | It is traditionally believed that chondrocytes and osteoblasts are two separate lineages with hypertrophic chondrocytes (HCs) being the terminal stage of chondrocyte differentiation, culminating in apoptosis. However, we have shown that HCs can contribute to the full osteoblast (Obs) lineage in vivo. MMP14 is a transmembrane matrix metalloproteinase responsible for matrix remodeling that is highly expressed at the chondro‐osseous junction which coincides with the transition from HCs to Obs. Knockout of Mmp14 in mice results in impaired endochondral ossification. To test whether loss of MMP14 has an impact on the HC to Obs transition, we have employed a genetic recombination approach to track and compare the fate of HCs in wild‐type and Mmp14 conditional and total null mutants. Both complete and conditional deletion of MMP14 activity results in increased number of HC‐descendent cells in the trabecular bone. Surprisingly, conditional knockout of Mmp14 in HC‐descendent cells results in increased trabecular bone formation. Our results suggest that MMP14 in general negatively regulates HC to Obs transition. | - |
dc.language | eng | en_US |
dc.publisher | The Chinese University of Hong Kong. | - |
dc.relation.ispartof | Hong Kong Inter-University 2013 Biochemistry Postgraduate Symposium | en_US |
dc.title | MMP14 regulates the lineage progression of hypertrophic chondrocytes | en_US |
dc.type | Conference_Paper | en_US |
dc.identifier.email | Chu, TL: chutl@hku.hk | en_US |
dc.identifier.email | Tsang, KY: kytsang@hku.hk | en_US |
dc.identifier.email | Tsang, SW: biotsw@hkucc.hku.hk | en_US |
dc.identifier.email | Zhou, Z: zhongjun@hkucc.hku.hk | en_US |
dc.identifier.email | Cheah, KSE: hrmbdkc@hku.hk | - |
dc.identifier.authority | Zhou, Z=rp00503 | en_US |
dc.identifier.authority | Cheah, KSE=rp00342 | en_US |
dc.description.nature | postprint | - |
dc.identifier.hkuros | 224443 | en_US |
dc.identifier.hkuros | 240452 | - |
dc.publisher.place | Hong Kong | - |