Conclusion
miR-200b-3p targeted CD36 to regulate cardiocyte apoptosis of DCM by activating PPAR-γ signaling pathway.
Methods
Bioinformatic analysis was used to analyze differentially expressed microRNA (miRNAs), messenger RNAs (mRNAs) and activated pathways in DCM. And then quantitative real-time polymerase chain reaction (qRT-PCR) was conducted to verify expression of miR-200b-3p and CD36 in DCM model rats and glucose treated H9c2 cell line. Luciferase reporter assay was used to verify the transcriptional regulation of agomiR-200b-3p and investigate the relationship between miR-200b-3p and CD36. Flow cytometry was performed to assess cardiocyte apoptosis in different interference conditions. Echocardiography was used to illustrate the ejection fraction rate and fraction shortening rate of DCM model rats. Next, hematoxylin-eosin (H&E) staining assay was carried out to reveal structures of cardiocyte tissues with transfection in different conditions. Masson trichrome staining was used to evaluate myocardial fibrosis. Western blot analysis was used to detect the expression levels of PPAR-γ signaling-related protein PPAR-γ and Bcl-2.
Objective
Current study focused on the influence of miR-200b-3p on cardiocyte apoptosis of diabetic cardiomyopathy (DCM) by regulating CD36 and peroxisome proliferator-activated receptor γ (PPAR-γ) signaling pathway.
Results
miR-200b-3p was low-expressed while CD36 was overexpressed in DCM. AgomiR-200b-3p could inhibit the expression of CD36 to regulate cardiocyte apoptosis in DCM. CD36 activated PPAR-γ signaling pathway in DCM. Silencing CD36 or GW9662 treatment protect rat against DCM.