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Articular cartilage damage can lead to joint deformity, pain, and severe dysfunction. However, due to the lack of blood vessels and nerves in articular cartilage, the self‐healing capacity of damaged cartilage is limited. In this study, we overexpressed small ubiquitin‐like modifier (SUMO)1, SUMO2/3, and SUMO1/2/3 in bone marrow mesenchymal stem cells (BMSCs). Then, these cells were inoculated on surfaces of different hardness, and their differentiation into chondrocytes, hypoxic tolerance ability, and inflammatory response was detected. Finally, BMSCs were transplanted into the injured knee joint cavity of the rats, and the repair was evaluated. We found that BMSCs overexpressing SUMO1 were more likely to differentiate into articular cartilage along with the hardness of the surface, while BMSCs overexpressing SUMO2/3 could reduce inflammation response and improve the damaged cartilage microenvironment. In the rat model, BMSCs overexpressing SUMO1/2/3 transplanted on injured articular cartilage surface showed better survival, less inflammatory response, and improved tissue repair capability. In conclusion, BMSCs overexpressing SUMO are more tolerant to hypoxia conditions, and have stronger repair ability for damaged chondrocytes in vitro and for articular cartilage injury model in rats, and are excellent seed cells for repairing articular cartilage. [ABSTRACT FROM AUTHOR]

Multiple sclerosis (MS) is an inflammatory and demyelinating disease of the central nervous system (CNS) that leads to disability in middle‐aged individuals. High rates of apoptosis and inappropriate homing are limitations for the application of stem cells in cell therapy. Preconditioning of bone marrow mesenchymal stem cells (BMSCs) with stromal cell‐derived factor 1α (SDF‐1α), also called C‐X‐C motif chemokine 12 (CXCL12), is an approach for improving the functional features of the cells. The aim of this study was to investigate the therapeutic efficacy of intranasal delivery of SDF‐1α preconditioned BMSCs in the cuprizone‐induced chronically demyelinated mice model. BMSCs were isolated, cultured, and preconditioned with SDF‐1α. Then, intranasal delivery of the preconditioned cells was performed in the C57BL/6 mice receiving cuprizone for 12 weeks. Animals were killed at 30 days after cell delivery. SDF‐1α preconditioning increased C‐X‐C chemokine receptor type 4 (CXCR4) expression on the surface of BMSCs, improved survival of the cells, and decreased their apoptosis in vitro. SDF‐1α preconditioning also improved CXCL12 level within the brain, and enhanced spatial learning and memory (assessed by Morris water maze [MWM]), and myelination (assessed by Luxol fast blue [LFB] and transmission electron microscopy [TEM]). In addition, preconditioning of BMSCs with SDF‐1α reduced the protein expressions of glial fibrillary acidic protein and ionized calcium‐binding adapter molecule (Iba‐1) and increased the expressions of oligodendrocyte lineage transcription factor‐2 (Olig‐2) and adenomatous polyposis coli (APC), evaluated by immunofluorescence. The results showed the efficacy of intranasal delivery of SDF‐1α‐preconditioned BMSCs for improving remyelination in the cuprizone model of MS. [ABSTRACT FROM AUTHOR]

While the ability of stem cells to switch lineages has been suggested, the route(s) through which this may happen is unclear. To date, the best characterized adult stem cell population considered to possess transdifferentiation capacity is BM-MSCs (bone marrow mesenchymal stem cells). We investigated whether BM-MSCs that had terminally differentiated into the neural or epithelial lineage could be induced to transdifferentiate into the other phenotype in vitro. Our results reveal that neuronal phenotypic cells derived from adult rat bone marrow cells can be switched to epithelial phenotypic cells, or vice versa, by culture manipulation allowing the differentiated cells to go through, first, dedifferentiation and then redifferentiation to another phenotype. Direct transdifferentiation from differentiated neuronal or epithelial phenotype to the other differentiated phenotype cannot be observed even when appropriate culture conditions are provided. Thus, dedifferentiation appears to be a prerequisite for changing fate and differentiating into a different lineage from a differentiated cell population. [ABSTRACT FROM AUTHOR]

Abstract: Hepatocyte-like cells induced from bone marrow mesenchymal stem cells (BMSCs) recover liver function in animal models with liver failure. Our initial findings revealed that human BMSCs improved liver function in hepatitis B patients with end stage liver disease. However, the susceptibility of BMSCs to HBV infection during induction toward hepatocytes remains unknown. We have assessed whether BMSCs-derived hepatocyte-like cells can function like liver cells and be infected by HBV. A new and efficient way to direct the differentiation of BMSCs into functional hepatocytes was developed. BMSCs obtained from hepatitis B patients were induced to differentiate into hepatocytes through exposure to HGF, FGF-4, and EGF. After 6 days of exposure, BMSCs-derived hepatocyte-like cells that expressed a subset of hepatic genes and showed hepatic functions were obtained. HBV was used to infect the differentiated cells, and subsequently these cells were assayed for the presence of HBeAg, HBsAg, and HBV DNA. BMSCs proved resistant to HBV infection, both in vitro and during differentiation into hepatocytes in vitro. This demonstrates that BMSCs are resistant to HBV infection. BMSCs are viable for transplantation and should facilitate further research exploring the in vivo HBV-resistance of the hepatocytes derived from BMSCs after transplantation, a characteristic that could form the basis for hepatocyte transplantation. [Copyright &y& Elsevier]