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The purpose of this study was to regenerate a meniscus using a scaffold from a normal meniscus and mesenchymal stromal cells derived from bone marrow (BM-MSCs). Thirty Sprague-Dawley rat menisci were excised and freeze-thawed three times with liquid nitrogen to kill the original meniscal cells. Bone marrow was aspirated from enhanced green fluorescent protein transgenic Sprague-Dawley rats. BM-MSCs were isolated, cultured for 2 weeks, and 2 x 10(5) cells were then seeded onto the meniscal scaffolds. Using a fluorescent microscope and immunohistochemical staining, repopulation of enhanced green fluorescent protein positive cells was observed in the superficial zone of the scaffold after 1 week of culture, and then in the deep zone after 2 weeks. At 4 weeks, expression of extracellular matrices was detected histologically and expression of mRNA for aggrecan and type X collagen was detected. Stiffness of the cultured tissue, assessed by the indentation stiffness test, had increased significantly after 2 weeks in culture, and approximated the stiffness of a normal meniscus. From this study, we conclude that a scaffold derived from a normal meniscus seeded with BM-MSCs can form a meniscus approximating a normal meniscus.

The purpose of this study was to assess transplantation of regenerated menisci using scaffolds from normal allogeneic menisci and bone-marrow-derived mesenchymal stromal cells (BM-MSCs) of rats. We reported that scaffolds derived from normal menisci seeded with BM-MSCs in vitro could form meniscal tissues within 4 weeks. Then, we hypothesized that our tissues could be more beneficial than allogeneic menisci regarding early maturation and chondroprotective effect. Bone marrow was aspirated from enhanced green fluorescent protein transgenic rats. BM-MSCs were isolated and seeded onto scaffolds which were prepared from Sprague-Dawley rat menisci. After 4 weeks in coculture, the tissues were transplanted to the defect of menisci. Repopulation of BM-MSCs and expression of extracellular matrices were observed in the transplanted tissues at 4 weeks after surgery. At 8 weeks, articular cartilage in the cell-free group was more damaged compared to that in the cell-seeded group or the meniscectomy group.

Platelet-rich plasma (PRP) contains several growth factors, including platelet-derived growth factor (PDGF), transforming growth factor-β1 (TGF-β1), insulin-like growth factor-1 (IGF-1), and vascular endothelial growth factor (VEGF), that are associated with repair processes after central nervous system injury. Although PRP have been applied to some regenerative therapies, the regeneration effects of PRP on spinal cord injury have not been reported. This study applied a rat organ coculture system to examine the ability of PRP to enhance axonal growth in spinal cord tissues and to identify the growth factors in PRP that contribute to the regulation of axon growth. PRP from human peripheral blood was added to organ cocultures. Furthermore, neutralizing antibodies against PDGF-AB, TGF-β1, IGF-1, or VEGF were added to the cocultures with PRP. Axon growth from the brain cortex into the spinal cord was assessed quantitatively using anterograde axon tracing with DiI. Addition of PRP to the cocultures promoted axon growth, and the axon growth was significantly suppressed by the addition of neutralizing antibodies against IGF-1 and VEGF, but not PDGF-AB. In contrast, axon growth was promoted significantly by the addition of neutralizing antibodies against TGF-β1. These findings indicate that PRP promotes axon growth in spinal cord tissues through mechanisms associated with IGF-1 and VEGF, and that TGF-β1 in PRP exerts negative effects on axon growth.