ABSTRACT
Objective To investigate the role of Wnt/β-catenin signaling pathway in the process of adipose-derived stem cells (ADSCs)differentiating into neurons.Methods The third generation of ADSCs were divided into three groups.Neural induction medium was used in induction group and DDK-1 was added into neural induction medium in inhibition group.Normal culture medium was used in control group.Ten days after culture,Real-time PCR and Western blot were used to detect the expressions of NSE,β-catenin and GSK-3βin each group.Results The expressions of NSE and β-catenin were high but the expression of GSK-3 was low in induction group.The expression ofβ-catenin was lower but GSK-3 was higher in inhibition group;the expression of NSE was much lower than that in induction group,but higher than control group.Conclusion The differentiation of ADSCs into neurons is related to activation of Wnt signaling pathway,but Wnt signal pathway is not the only pathway to regulate ADSCs differentiation which may be controlled by different signaling pathways.
ABSTRACT
Objective To investigate the role of Wnt/β-catenin signaling pathway in the process of adipose-derived stem cells (ADSCs)differentiating into neurons.Methods The third generation of ADSCs were divided into three groups.Neural induction medium was used in induction group and DDK-1 was added into neural induction medium in inhibition group.Normal culture medium was used in control group.Ten days after culture,Real-time PCR and Western blot were used to detect the expressions of NSE,β-catenin and GSK-3βin each group.Results The expressions of NSE and β-catenin were high but the expression of GSK-3 was low in induction group.The expression ofβ-catenin was lower but GSK-3 was higher in inhibition group;the expression of NSE was much lower than that in induction group,but higher than control group.Conclusion The differentiation of ADSCs into neurons is related to activation of Wnt signaling pathway,but Wnt signal pathway is not the only pathway to regulate ADSCs differentiation which may be controlled by different signaling pathways.
ABSTRACT
<p><b>OBJECTIVE</b>To explore the effect and mechanism of Poly I:C in inducing growth inhibition and apoptosis of human hepatocellular carcinoma SMMC-7721 cells.</p><p><b>METHODS</b>SMMC-7721 cells were treated with different doses of Poly I:C for 24, 48, and 72 h, and the cell growth inhibition rate was analyzed with CCK-8 assay. The cell cycle and the apoptosis were analyzed using flow cytometry with Annexin-V and PI staining, and quantitative RT-PCR analysis were used to detect the expression of TLR3, TRIF, and IFN-beta mRNA in cells.</p><p><b>RESULTS</b>In the cells exposed to Poly I:C at low, moderate, and high doses, the inhibitory rates was the highest in high-dose Poly I:C group, and at a given Poly I:C dose, prolonged exposure resulted in significantly increased cell growth inhibition rate (P<0.05). Flow cytometry showed that Poly I:C induced cell apoptosis in a time- and dose-dependent manner and significantly increased the percentage of G1-phase cells as compared with that in the control group. The mRNA level of TLR3, TRIF, and IFN-beta were also increased following Poly I:C treatment in comparison with the control group.</p><p><b>CONCLUSION</b>Poly I:C can induce significant growth inhibition and apoptosis of SMMC-7721 cells in a dose- and time-dependent manner possibly by causing cell cycle arrest and TLR3 signaling pathway activation that leads to IFN-beta production and cell apoptosis.</p>