The effects of microRNA-126 reduced inflammation and apoptosis of diabetic nephropathy through PI3K/AKT signalling pathway by VEGF

Arch Physiol Biochem. 2022 Oct;128(5):1265-1274. doi: 10.1080/13813455.2020.1767146. Epub 2020 May 25.

Abstract

Gene expression microarray and reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to measure the expression of miR-126. In model of diabetic nephropathy, we demonstrated that miR-126 expression was down-regulated, compared with control group. Down-expression of miR-126 promoted cell apoptosis and increased inflammation (as indicated by the levels of IL-1β, IL-6, IL-18 and TNF-α) of diabetic nephropathy in vitro. miR-126 over-expression led to significant inhibition of cell apoptosis and suppressed inflammation (IL-1β, IL-6, IL-18 and TNF-α). However, the down-expression of miR-126 suppressed the protein expression of VEGF, PI3K and p-AKT in diabetic nephropathy in vitro. On the contrary, over-expression of miR-126 induced the protein expression of VEGF, PI3K and p-AKT in diabetic nephropathy in vitro. The inhibition of VEGF increased the effect of miR-126 down-expression on apoptosis and inflammation in diabetic nephropathy in vitro. We investigated the specific function of miR-126 in patients with diabetic nephropathy and its possible mechanism.

Keywords: AKT; MicroRNA-126; PI3K; VEGF; diabetic nephropathy.

MeSH terms

  • Apoptosis
  • Cell Proliferation
  • Diabetes Mellitus*
  • Diabetic Nephropathies* / genetics
  • Humans
  • Inflammation / genetics
  • Interleukin-18
  • Interleukin-6
  • MicroRNAs* / genetics
  • MicroRNAs* / metabolism
  • Phosphatidylinositol 3-Kinases / metabolism
  • Proto-Oncogene Proteins c-akt / metabolism
  • Tumor Necrosis Factor-alpha / metabolism
  • Vascular Endothelial Growth Factor A / genetics
  • Vascular Endothelial Growth Factor A / metabolism

Substances

  • Interleukin-18
  • Interleukin-6
  • MIRN126 microRNA, human
  • MicroRNAs
  • Tumor Necrosis Factor-alpha
  • Vascular Endothelial Growth Factor A
  • Proto-Oncogene Proteins c-akt