Exogenous collagen-enhanced recruitment of mesenchymal stem cells during rabbit articular cartilage repair
DOI:
https://doi.org/10.1080/17453670710014653Abstract
Background Despite the well-known effect of type-I collagen in promoting cartilage repair, the mechanism still remains unknown. In this study we investigated this mechanism using a rabbit model of cartilage defects. Animals and methods 5-mm-diameter full-thickness defects were created on both patellar grooves of 53 Japanese white rabbits (approximately 13 weeks old). The left defect was filled with collagen gel and the right defect was left empty. The rabbits were killed and examined morphometrically until the twenty-fourth postoperative week, by (1) evaluation of matrix production, (2) enumeration of the total number of cells engaged in cartilage repair, (3) enumeration of the proliferating cells, (4) localization of mesenchymal stem cells, and (v) localization of apoptotic cells. Results We found that type-I collagen enhances cell recruitment, and thereby increases the number of proliferating cells. A considerable proportion of the proliferating cells were identified as bone marrow-derived mesenchymal stem cells. However, type-I collagen does not prevent the chondrocyte precursors from undergoing apoptotic disengagement from the chondrogenic lineage. Interpretation Type-I collagen promotes cartilage repair by enhancing recruitment of bone marrowderived mesenchymal stem cells. Additional use of agent(s) that sustain mesenchymal stem cells along the chondrogenic path of differentiation may constitute an appropriate environment for cartilage repair.Downloads
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Published
2007-01-01
How to Cite
Kubo, M., Imai, S., Fujimiya, M., Isoya, E., Ando, K., Mimura, T., & Matsusue, Y. (2007). Exogenous collagen-enhanced recruitment of mesenchymal stem cells during rabbit articular cartilage repair. Acta Orthopaedica, 78(6), 845–855. https://doi.org/10.1080/17453670710014653
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Acta Orthopaedica (Scandinavica) content is available freely online as from volume 1, 1930. The journal owner owns the copyright for all material published until volume 80, 2009. As of June 2009, the journal has however been published fully Open Access, meaning the authors retain copyright to their work. As of June 2009, articles have been published under CC-BY-NC or CC-BY licenses, unless otherwise specified.