Human Cartilage-Derived Progenitors Resist Terminal Differentiation and Require CXCR4 Activation to Successfully Bridge Meniscus Tissue Tears.
dc.contributor.author | Jayasuriya, Chathuraka T | |
dc.contributor.author | Twomey-Kozak, John | |
dc.contributor.author | Newberry, Jake | |
dc.contributor.author | Desai, Salomi | |
dc.contributor.author | Feltman, Peter | |
dc.contributor.author | Franco, Jonathan R | |
dc.contributor.author | Li, Neill | |
dc.contributor.author | Terek, Richard | |
dc.contributor.author | Ehrlich, Michael G | |
dc.contributor.author | Owens, Brett D | |
dc.date.accessioned | 2022-10-06T17:37:26Z | |
dc.date.available | 2022-10-06T17:37:26Z | |
dc.date.issued | 2019-01 | |
dc.date.updated | 2022-10-06T17:37:10Z | |
dc.description.abstract | Meniscus injuries are among the most common orthopedic injuries. Tears in the inner one-third of the meniscus heal poorly and present a significant clinical challenge. In this study, we hypothesized that progenitor cells from healthy human articular cartilage (chondroprogenitor cells [C-PCs]) may be more suitable than bone-marrow mesenchymal stem cells (BM-MSCs) to mediate bridging and reintegration of fibrocartilage tissue tears in meniscus. C-PCs were isolated from healthy human articular cartilage based on their expression of mesenchymal stem/progenitor marker activated leukocyte cell adhesion molecule (ALCAM) (CD166). Our findings revealed that healthy human C-PCs are CD166+, CD90+, CD54+, CD106- cells with multilineage differentiation potential, and elevated basal expression of chondrogenesis marker SOX-9. We show that, similar to BM-MSCs, C-PCs are responsive to the chemokine stromal cell-derived factor-1 (SDF-1) and they can successfully migrate to the area of meniscal tissue damage promoting collagen bridging across inner meniscal tears. In contrast to BM-MSCs, C-PCs maintained reduced expression of cellular hypertrophy marker collagen X in monolayer culture and in an explant organ culture model of meniscus repair. Treatment of C-PCs with SDF-1/CXCR4 pathway inhibitor AMD3100 disrupted cell localization to area of injury and prevented meniscus tissue bridging thereby indicating that the SDF-1/CXCR4 axis is an important mediator of this repair process. This study suggests that C-PCs from healthy human cartilage may potentially be a useful tool for fibrocartilage tissue repair/regeneration because they resist cellular hypertrophy and mobilize in response to chemokine signaling. Stem Cells 2019;37:102-114. | |
dc.identifier.issn | 1066-5099 | |
dc.identifier.issn | 1549-4918 | |
dc.identifier.uri | ||
dc.language | eng | |
dc.publisher | Oxford University Press (OUP) | |
dc.relation.ispartof | Stem cells (Dayton, Ohio) | |
dc.relation.isversionof | 10.1002/stem.2923 | |
dc.subject | Cartilage, Articular | |
dc.subject | Animals | |
dc.subject | Humans | |
dc.subject | Rats | |
dc.subject | Receptors, CXCR4 | |
dc.subject | Cell Differentiation | |
dc.subject | Chondrogenesis | |
dc.subject | Meniscus | |
dc.title | Human Cartilage-Derived Progenitors Resist Terminal Differentiation and Require CXCR4 Activation to Successfully Bridge Meniscus Tissue Tears. | |
dc.type | Journal article | |
duke.contributor.orcid | Li, Neill|0000-0001-9149-4859 | |
pubs.begin-page | 102 | |
pubs.end-page | 114 | |
pubs.issue | 1 | |
pubs.organisational-group | Duke | |
pubs.organisational-group | School of Medicine | |
pubs.organisational-group | Clinical Science Departments | |
pubs.organisational-group | Orthopaedic Surgery | |
pubs.publication-status | Published | |
pubs.volume | 37 |
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