No abstract

Human adipose-derived mesenchymal stem cells (MSCs) were differentiated into chondrogenic MSCs, and fibrin glue was used together to explore the feasibility of whether cartilages can be generated in vivo by injecting the differentiated cells. Mesenchymal stem cells extracted from human adipose were differentiated into chondrogenic MSCs, and such differentiated cells mixed with fibrin glue were injected subcutaneously into the back of the nude mouse. In addition to visual evaluation of the tissues formed after 4, 8, and 12 weeks, hematoxylin-eosin staining, Masson trichrome staining, measurement of glycosaminoglycan concentration using dimethylmethylene blue, agreecan through reverse transcriptase-polymerase chain reaction, type II collagen, and expression of SOX-9 were verified. Moreover, the results were compared with 2 groups of controls: 1 control group that received only injection of chondrogenic-differentiated MSC and the supporting control group that received only fibrin glue injection. For the experimental group, cartilage-like tissues were formed after 4, 8, and 12 weeks. Formation of cartilage tissues was not observed in any of 4, 8, and 12 weeks of the control group. The supporting control group had only a small structure formation after 4 weeks, but the formed structure was completely decomposed by the 8th and 12th weeks. The range of staining dramatically increased with time at 4, 8, and 12 weeks in Masson trichrome staining. The concentration of glycosaminoglycan also increased with time. The increased level was statistically significant with more than 3 times more after 8 weeks compared with 4 weeks and more than 2 times more after 12 weeks compared with 8 weeks. Also, in reverse transcriptase-polymerase chain reaction at 4, 8, and 12 weeks, all results expressed a cartilage-specific gene called aggrecan, type II collagen, and SOX-9. The study verified that the chondrogenic-differentiated MSCs derived from human adipose tissues with fibrin glue can proliferate and form new cartilage. Our findings suggest that formation of cartilages in vivo is possible.

To investigate whether diabetes mellitus affects the wound‐healing‐promoting potential of adipose tissue‐derived stem cells, we designed a wound‐healing model using diabetic mice. We compared the degree of wound healing between wounds treated with normal adipose tissue‐derived stem cells and wounds treated with diabetic adipose tissue‐derived stem cells. We evaluated the wound‐healing rate, the epithelial tongue distance, the area of granulation tissue, the number of capillary and the number of Ki‐67‐stained cells. The wound‐healing rate was significantly higher in the normal adipose tissue‐derived stem cells group than in the diabetic adipose tissue‐derived stem cells group; it was also significantly higher in the normal adipose tissue‐derived stem cells group than in the control group. Although the diabetic adipose tissue‐derived stem cells group showed a better wound‐healing rate than the control group, the difference was not statistically significant. Similar trends were observed for the other parameters examined: re‐epithelisation and keratinocyte proliferation; granulation tissue formation; and dermal regeneration. However, with regard to the number of capillary, diabetic adipose tissue‐derived stem cells retained their ability to promote neovasculisation and angiogenesis. These results reflect the general impairment of the therapeutic potential of diabetic adipose tissue‐derived stem cells in vivo.

In this study, the authors investigated the effects of adipose-derived stromal cells (ADSCs) and of their extract on wound healing. After creating wound healing splint model on the backs of mice, ADSCs and their extract were applied. Wound healing rates were calculated at 3, 5, 7, 10, and 14 days after the wounding, and tissues were harvested at 7 and 14 days for histological analysis. Wound healing rates were significantly higher at 7, 10, and 14 days in the cell group than in the control, but in the cell extract group wound healing rates were significantly decreased (P<0.05). Histological scores and capillary densities in the cell group were significantly higher at 2 weeks (P<0.05). In the cell group, thick inflammatory cell infiltration and many capillaries were observed at 1 week, and thick epithelium and numerous large capillaries were observed at 2 weeks. The present study suggests that ADSCs accelerate wound healing as known, and the effects of ADSCs on wound healing may be due to replacing insufficient cells by differentiation of ADSCs in the wound and secreting growth factors by differentiated cells, and not due to the effect of factors within ADSCs.