MiR-205 influences renal injury in sepsis rats through HMGB1-PTEN signaling pathway

Eur Rev Med Pharmacol Sci. 2019 Dec;23(24):10950-10956. doi: 10.26355/eurrev_201912_19798.

Abstract

Objective: To investigate the influences of micro ribonucleic acid (miR)-205 on renal injury in sepsis rats through the high-mobility group box 1 (HMGB1)-phosphatase and tensin homolog deleted on chromosome ten (PTEN) signaling pathway.

Materials and methods: A rat model of sepsis-induced renal injury was established by cecal ligation and perforation. The rats were randomly divided into 3 groups, namely the Sham group, the Model group, and the miR-205 group. Hematoxylin and eosin (HE) staining was applied to examine the pathological renal morphology. The enzyme-linked immunosorbent assay (ELISA) was adopted to measure the serum levels of Caspase-3 and Bcl-2-associated X protein (Bax) in rats. Cell apoptosis rate in the renal tissues was detected via terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay. Finally, the protein levels of phosphorylate-HMGB1 (p-HMGB1) and p-PTEN in the renal tissues were determined using the Western blotting (WB) assay.

Results: Compared with those in the Sham group, the pathological morphology of the renal tissues was poor in Model group. The serum levels of Caspase-3 and Bax, the apoptosis rate, and the protein levels of p-HMGB1 and p-PTEN were remarkably enhanced in the Model group compared to the Sham group. In comparison with those in Model group, the pathological changes in renal morphology, apoptosis-related indexes, and protein levels of p-HMGB1 and p-PTEN were alleviated in the miR-205 group.

Conclusions: MiR-205 agonist can improve the pathological morphology in the sepsis rats with renal injury, improve renal cell apoptosis, and inhibit the protein levels of HMGB1 and PTEN in renal tissues. MiR-205 alleviates sepsis-induced renal injury through the HMGB1-PTEN signaling pathway.

MeSH terms

  • Acute Kidney Injury / metabolism*
  • Acute Kidney Injury / pathology
  • Animals
  • Apoptosis
  • Cell Proliferation
  • Disease Models, Animal
  • HMGB1 Protein / analysis
  • HMGB1 Protein / metabolism*
  • Male
  • MicroRNAs / metabolism*
  • PTEN Phosphohydrolase / analysis
  • PTEN Phosphohydrolase / metabolism*
  • Phosphorylation
  • Rats
  • Rats, Sprague-Dawley
  • Sepsis / metabolism*
  • Sepsis / pathology
  • Signal Transduction*

Substances

  • HMGB1 Protein
  • Hbp1 protein, rat
  • MIRN205 microRNA, rat
  • MicroRNAs
  • PTEN Phosphohydrolase
  • Pten protein, rat