The Research Of The Tropism Of Menstrual Stem Cells Tending To U87 Cells In Vitro

Our research is to investigate the tropism of MenSC to U87 cells and try to find out the internal molecule mechanism.Firstly,we investigate that whether the SDF-1α could affect the tropism of MenSC to U87 cells.We conclude that when the concentration of SDF-1α increses, the tropism of MenSC to U87 cells enhances. Moreover,after we knock down the expression of CXCR4/7 in MenSC,we found that the tropism capacity of the MenSC declines significantly. It can be seen that SDF-1α/CXCR4 signaling pathway plays an important role in mediating the tropism of MenSC toward U87 cells.Secondly, We respectively detect the related protein expression in MenSC in 0min,1min,5min,15min,30min,60min after we put 100ng/ml SDF-1α in MenSC,.we find that the expression level of p-Jak2 and p-STAT3 reach the hignest level in five minutes immediately and remain steady later after we put the SDF-1α in MenSC.The expression level of p-ERK1/2 increases the hignest level in 30 minutes and keeps steady later.The expression level of p-AKT increases the hignest level in 5 minutes and falls to a stable state later. Moreover,We investigate the tropism capacity of the MenSC in which the Jak2/STAT3 and ERK signaling pathway are blocked down. All the above results indicate that the tropism capacity of the MenSC are weaken enormously when the Jak2/STAT3 signaling pathway is blocked down and inhibited partly when the ERK1/2 signaling pathway is blocking down. In conclusion,we indicate that the Jak/STAT3 and ERK 1/2 signaling pathway play an important role in the tropism of the MenSC toward U87 cells.Lastly,We respectively detect the related skeleton protein expression in MenSC and cytoskeleton flurescence detection in 0min,1min,5min,15min,30min,60min after we put 100ng/ml SDF-1α in MenSC. We find that the expression level of p-FAK increases immediately and keeps steady later after we put the SDF-1α in MenSC. The expression level of p-Paxillin reaches hignest level in 15minutes and remains unchanged later. The extension of cytoskeleton strengthens gradually to the largest in 15minutes and remain unchanged later. On the contrary,we investigate that the related skeleton protein expression in MenSC and cytoskeleton flurescence detection after we put the Jak2/STAT3 inhibitor and ERK inhibitor. We conclude that the both inhibitors can weaken the expression of p-STAT3 and p-ERK1/2 significantly and restrain the stretch of the cytoskeleton in MenSC.In summary,our study demonstrates that SDF-la binds to its cognate receptors CXCR4/7 to active Jak2/STAT3 and ERK1/2 signaling pathway,which in turn modulates FAK and Paxillin that induce reorganization of actin cytoskeleton, thereby promoting MenSC migration. Based on these results, we suggest that SDF-1α/CXCR4,Jak2/STAT3 and ERK signaling pathway play an important role in the tropism of the MenSC toward the U87 cells.