ABSTRACT
Objective To investigate the renoprotective effects of autologous transplantation of adipose-derived mesenchymal stem cells (ADMSCs) in diabetic rats. Methods Sprague-Dawley (SD) rats were injected intraperitoneally with 40 mg/kg streptozotocin (STZ) for 5 consecutive days to induce type 1 diabetes. Four weeks following STZ injection, eighteen SD rats were randomized into two groups: the diabetic group (n = 9) and the ADMSCs group (n = 9). Normal nondiaetic rats were set as the normal control (n = 9). Autologous ADMSCs were cultured and identified in vitro , which were intravenously injection to the ADMSCs group rats via the tail vein. At 8 weeks after transplantation, levels of blood glucose, insulin, serum urea nitrogen, serumcreatinine and urine protein were measured. Meanwhile the body weight and kidney weight were examined. Results Mesenchymal cell surface markers were expressed in the cultured ADMSCs. The ADMSCs could differentiate into the adipogenic and osteoblastic lineages. Both the diabetic group and the ADMSCs group rats had higher levels of blood glucose , urea nitrogen , serum creatinine , urine protein and higher ratio of the kidney weight/body weight than those in the normal control group (P < 0.05, respectively). Blood glucose, urea nitrogen and the ratio of kidney weight/body weight in the ADMSCs group rats were significantly decreased compared with the diabetic group (P < 0.05, respectively). The decreased insulin level was attenuated after transplantation of ADMSCs (P < 0.05). Besides, levels of serum creatinine and urine protein in the ADMSCs group were lower than those in the diabetic group with no significant difference. Conclusion Autologous transplantation of ADMSCs can improve metabolic disorder and relieves diabetic renal damage.
ABSTRACT
Objective To investigate the roles of P53/P21 during neuronal differentiation with a differentiated model of PC12 cells. Methods A new cell line PC12(P53/m175) was created by stable transfection of a retrovirus plasmid pBabe-P53/m175, which contains a dominant-negative P53 gene mutant. After NGF treatment, observing with phase-contrast microscopy, flow cytometric analysis and western blotting of P53 and P21 were performed. Results Expression of P53 and P21 was obviously increased in NGF-induced PC12 cells. The appearance of cell cycle G1 phase arrest paralleled the increased expressions of P53 and P21. The level of P21 protein did not change after treatment with NGF in PC12(P53/m175) cells and the extent of G1 phase arrest markedly decreased. However, we did find the normal neurite outgrowth in NGF-treated PC12(P53/m175) cells. Conclusion NGF-induced an increased protein levels of P53 and its transcriptional element, P21 is essential for cell cycle G1 phase arrest, but does not necessarily correlate with the neurite outgrowth of PC12 cells.