Activation Of Peroxisome Proliferator-activated Receptor-γ Induces Declined Cell Activity Through Wnt Signal Pathway In Osteoblastic MC3T3-E1Cells

Objective To investigate the effects of pioglitazone and rosiglitazone on osteoblasticMC3T3-E1cells proliferation and apoptosis, as well as the crosstalk between PPARγand Wnt signal pathway, demonstrate the mechanism through which PPARγ agonisteffects the activity of osteoblast.Methods MC3T3-E1cell were treated with0，10,20,30,40μM pioglitazone androsiglitazone for24h, the groups of20μM followed with the intervene ofrecombination mouse Wnt3a protein(50ng/ml) for6h. Cell activity was measured byMTT, cell apoptosis were inspected with flow cytometry, effect on level of LRP5/6,GSK3β, TCF7L2, PPARγ, cyclinD1mRNA were identified by RT-PCR, and theprotein level of β-catenin and p-GSK3β were detected by western blot.Results With the intervene of Pio and Rosi, the proliferate activity of the cellsdecreases while the apoptosis rate increases, there is no significant difference betweenPio and Rosi; They can negative regulate the protein level of β-catenin and positiveregulate p-GSK3β, but the mRNAlevel of LRP5/6, GSK3β, TCF7L2wereinvariant. It seems the the activate of PPARγ accompanied the suppression of Wntsignal pathway. We activate the Wnt pathway after the activation of PPARγ through the intervene of Wnt3a protein, detected the proliferate activity of the cells increaseswhile the apoptosis rate decreases, comparing with the control groups, the proteinlevel of β-catenin up regulated as the p-GSK3β down regulated. Activating Wnt signalpathway would suppress the activity alter of osteoblast by PPARγ.Conclusion Pio and Rosi can inhibit the proliferate activity of MC3T3-E1cells andpromote cell apoptosis, there performances no significant difference between the two.Activation of PPARγ induces declined cell activity through Wnt signal pathway inosteoblastic MC3T3-E1cells.