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Article: Mesenchymal stem cells reduce intervertebral disc fibrosis and facilitate repair

TitleMesenchymal stem cells reduce intervertebral disc fibrosis and facilitate repair
Authors
Issue Date2014
Citation
Stem Cells, 2014, v. 8, p. 2164-2177 How to Cite?
AbstractIntervertebral disc degeneration is associated with back pain and radiculopathy which, being a leading cause of disability, seriously affects the quality of life and presents a hefty burden to society. There is no effective intervention for the disease and the aetiology remains unclear. Here, we show that disc degeneration exhibits features of fibrosis in humans and confirmed this in a puncture-induced disc degeneration (PDD) model in rabbit. Implantation of bone marrow-derived mesenchymal stem cells (MSCs) to PDD discs can inhibit fibrosis in the nucleus pulposus with effective preservation of mechanical properties and overall spinal function. We showed that the presence of MSCs can suppress abnormal deposition of collagen I in the nucleus pulposus, modulating profibrotic mediators MMP12 and HSP47, thus reducing collagen aggregation and maintaining proper fibrillar properties and function. As collagen fibrils can regulate progenitor cell activities, our finding provides new insight to the limited self-repair capability of the intervertebral disc and importantly the mechanism by which MSCs may potentiate tissue regeneration through regulating collagen fibrillogenesis in the context of fibrotic diseases.
Persistent Identifierhttp://hdl.handle.net/10722/198461

 

DC FieldValueLanguage
dc.contributor.authorLeung, VYLen_US
dc.contributor.authorAladin Kaderbatcha, DMen_US
dc.contributor.authorLv, Fen_US
dc.contributor.authorTam, Ven_US
dc.contributor.authorNgan, AHWen_US
dc.contributor.authorWu, EXen_US
dc.contributor.authorLuk, KDKen_US
dc.contributor.authorLu, WWen_US
dc.contributor.authorMasuda, Ken_US
dc.contributor.authorChan, Den_US
dc.date.accessioned2014-07-07T07:00:31Z-
dc.date.available2014-07-07T07:00:31Z-
dc.date.issued2014-
dc.identifier.citationStem Cells, 2014, v. 8, p. 2164-2177en_US
dc.identifier.urihttp://hdl.handle.net/10722/198461-
dc.description.abstractIntervertebral disc degeneration is associated with back pain and radiculopathy which, being a leading cause of disability, seriously affects the quality of life and presents a hefty burden to society. There is no effective intervention for the disease and the aetiology remains unclear. Here, we show that disc degeneration exhibits features of fibrosis in humans and confirmed this in a puncture-induced disc degeneration (PDD) model in rabbit. Implantation of bone marrow-derived mesenchymal stem cells (MSCs) to PDD discs can inhibit fibrosis in the nucleus pulposus with effective preservation of mechanical properties and overall spinal function. We showed that the presence of MSCs can suppress abnormal deposition of collagen I in the nucleus pulposus, modulating profibrotic mediators MMP12 and HSP47, thus reducing collagen aggregation and maintaining proper fibrillar properties and function. As collagen fibrils can regulate progenitor cell activities, our finding provides new insight to the limited self-repair capability of the intervertebral disc and importantly the mechanism by which MSCs may potentiate tissue regeneration through regulating collagen fibrillogenesis in the context of fibrotic diseases.en_US
dc.languageengen_US
dc.relation.ispartofStem Cellsen_US
dc.titleMesenchymal stem cells reduce intervertebral disc fibrosis and facilitate repairen_US
dc.typeArticleen_US
dc.identifier.emailLeung, VYL: vicleung@hku.hken_US
dc.identifier.emailAladin Kaderbatcha, DM: darwesh@hku.hken_US
dc.identifier.emailLv, F: fengjuan@hku.hken_US
dc.identifier.emailTam, V: vivtam@hku.hken_US
dc.identifier.emailNgan, AHW: hwngan@hkucc.hku.hken_US
dc.identifier.emailWu, EX: ewu1@hkucc.hku.hken_US
dc.identifier.emailLuk, KDK: hrmoldk@hkucc.hku.hken_US
dc.identifier.emailLu, WW: wwlu@hku.hken_US
dc.identifier.emailChan, D: chand@hku.hken_US
dc.identifier.authorityLeung, VYL=rp01764en_US
dc.identifier.authorityNgan, AHW=rp00225en_US
dc.identifier.authorityWu, EX=rp00193en_US
dc.identifier.authorityLuk, KDK=rp00333en_US
dc.identifier.authorityLu, WW=rp00411en_US
dc.identifier.authorityChan, D=rp00540en_US
dc.identifier.doi10.1002/stem.1717-
dc.identifier.hkuros230106en_US

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