Cer(d18:1/16:0)Promotes Mitochondrial Dysfunction and Fibrotic Phenotype Transformation in HK-2 Cells
Objective To explore the effect of Cer(d18:1/16:0),the core marker in the development of diabetic kidney disease(DKD),on mitochondrial dysfunction and phenotypic transformation of human renal proximal tubule cells(HK-2)induced by high glucose.Methods With the help of qRT-PCR technology,the expression of ceramide synthesis related enzymes in HK-2 cells stimulated by high glucose was detected at the transcription level.The effects of different concentrations of Cer(d18:1/16:0)on the viability of HK-2 cells were detected by CCK8 method.The changes of mitochondrial number in HK-2 cells stimulated by different concentrations of Cer(d18:1/16:0)were evaluated by mitochondrial fluorescent probe.Western blot was used to detect the expression of mitochondrial related proteins and fibrosis indexes before and after the administration of Cer(d18:1/16:0).Results The expression of Ceramide synthase 2,(CERS2)in HK-2 cells increased in high glucose environment.Exogenous Cer(d18:1/16:0)can significantly inhibit the viability of HK-2 cells,can reduce the total and average fluorescence intensity of mitochondria in HK-2 cells induced by high glucose.The protein expression of CV-ATP5A and CIII-UQCRC2 decreased,while the protein expression of Coll 3,MMP9 and α-SMA increased.Conclusion Cer(d18:1/16:0)can induce mitochondrial dysfunction and fibrotic phenotype transformation in HK-2 cells stimulated by high glucose.
Diabetic kidney diseaseCer(d18:1/16:0)HK-2 cellsPhenotypic transformation of fibrosisMitochondrial dysfunction
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