β-Arrestin 1/2 Aggravates Podocyte Apoptosis of Diabetic Nephropathy via Wnt/β-Catenin Pathway

Background β-arrestins have been shown to play a critical role in the progression of diabetic nephropathy. Nevertheless, the potential mechanism of β-arrestins on the regulation of podocyte apoptosis has rarely been discussed. This study aimed to elucidate the regulation of β-arrestin 1/2 on podocyte apoptosis through the Wnt/β-catenin pathway. Material/Methods This study structured β-arrestin 1/2 down-regulated and up-regulated expression by plasmid transfection. The protein levels were detected with Western blotting, and mRNA expression was detected with RT-qPCR. The apoptotic cells were measured by flow cytometry. Results β-arrestin 1/2 expression levels of podocytes were up-regulated in high-glucose-induced podocytes. β-arrestin 1/2 overexpression inhibited the expression of nephrin and podocin protein. Up-regulated β-arrestin 1/2 promoted podocyte apoptosis and p53 pathway by increasing Bax, cleaved caspase-3, and p-p53 levels in high-glucose-induced podocytes. Flow cytometry showed that the apoptotic cells were markedly higher in the β-arrestin 1/2 up-regulated group compared with the scramble group. Expression of β-catenin was increased in the β-arrestin 1/2 up-regulated group, which indicated that the Wnt/β-catenin pathway was activated. Wnt/β-catenin pathway inhibitor (Dkk1) distinctly suppressed the apoptosis induced by β-arrestin 1/2 overexpression and high glucose. Conclusions These results provide a molecular pathomechanism of β-arrestin 1/2 and Wnt/β-catenin pathway on podocyte apoptosis and provide new ideas for the treatment of diabetic nephropathy, which paves the way for the future study of diabetic nephropathy and podocytes.

• Publication year

  2018

• Venue

  Medical Science Monitor

• Publication date

  2018-03-24

• Fields of study

  Medicine, Chemistry

• Identifiers
  DOI 10.12659/MSM.905642PMID 29572435PMCID 5881455
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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