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Studies On The Effects Of PPARγ Induced By Wnt Signaling Pathway In NIT-1 β Cell

Posted on:2012-10-06Degree:MasterType:Thesis
Country:ChinaCandidate:B W ZhouFull Text:PDF
GTID:2214330362957354Subject:Internal Medicine
Abstract/Summary:PDF Full Text Request
Objective: To study the effect of peroxisome proliferator-activated receptorγ(PPARγ) and glucokinase(GK) induced by Wnt signaling pathway in mice NIT-1 pancreaticβcell, and to explore the interactional roles between PPARγand Wnt signaling pathways.Methods: Wnt signaling pathway can be activated by recombinated Wnt3a protein and blocked by dickkopf 1(DKK1), and phosphatidylinositol 3 kinase (PI3K) signaling pathway can be blocked by wortmannin(Wort) in NIT-1 cells. Cells were divided into four groups according to different interventions: control group, Wnt3a group, Wnt3a+DKK1 group and Wnt3a+Wort group. After 24 hour cultivation, mRNA levels of PPARγand GK were detected by fluorescent quantitation of realtime PCR. Western Blot was used to compare the protein levels of PPARγamong the different groups.Results: The mRNA and protein levels of PPARγwere elevated induced by the activation of Wnt pathway, and expression of GK gene also be stimulated. These effects were abrogated by inhibitions of Wnt or(and) PI3K, DKK1 or(and) Wort.Conclusions: These results indentified that PPARγand GK can be up-regulated by Wnt singnaling, and the effects might partially be PI3K-dependent.
Keywords/Search Tags:Wnt, PI3K, PPARγ, β-catenin, TCF7L2, Akt, GK
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