Mechanistic Study on the Regulation of Diabetes Kidney Disease by METTL3 through the miR-126-Mediated TGF-β/Smad Signaling Pathway
Objective:To establish a rat model of diabetic kidney disease(DKD)and explore the mechanism by which METTL3 regulates DKD.Methods:After 7 days of adaptive feeding,SD rats were ran-domly divided into four groups:normal control group(Control group),DKD model group(DKD group),DKD model + METTL3 interference control group(DKD+NC group),and DKD model + METTL3 interfer-ence group(DKD+siMETTL3 group),with 8 rats in each group.After modeling,blood specimens and kidney tissues were collected,and levels of fasting blood glucose(FBG),blood urea nitrogen(BUN),24-hour u-rine protein(UTP),gene expression of miR-126 using RT-qPCR,expression of TGF-β1 using ELISA,and protein levels of METTL3,smad2,smad3,and smad7 using Western blotting were analyzed by a fully auto-matic biochemical analyzer.Results:Compared to the control group,the DKD group showed significant in-creases in FBG,BUN,UTP,TGF-β1,METTL3,smad2,and smad3(P<0.05),and significant decreases in body weight,miR-126,and smad7(P<0.05).When compared to the DKD group,the DKD+siMETTL3 group exhibited significant decreases in FBG,BUN,UTP,TGF-β1,METTL3,smad2,and smad3(P<0.05),and significant increases in body weight,miR-126,and smad7(P<0.05).Conclusion:METTL3 can mediate the progression of DKD by regulating miR-126 and TGF-β/smad pathway.
万方数据
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