High glucose and TGF-β1 reduce expression of endoplasmic reticulum-resident selenoprotein S and selenoprotein N in human mesangial cells

Ren Fail. 2019 Nov;41(1):762-769. doi: 10.1080/0886022X.2019.1641413.

Abstract

There are seven endoplasmic reticulum (ER)-resident selenoproteins in human body and they can regulate the inflammation, oxidative stress, and ER stress. We established transforming growth factor-β1 (TGF-β1) or high glucose (HG) induced human mesangial cells (HMCs) fibronectin expression model in vitro. Next, the expression changes of seven ER-resident selenoproteins were detected under HG conditions and we found selenoprotein S (SELENOS), selenoprotein N (SELENON) were significantly down-regulated but selenoprotein M was significantly up-regulated in transcription level. Furthermore, we found that TGF-β1 and HG down-regulated the expression of SELENOS and SELENON in a time- and dose-dependent manner, respectively. Finally, SELENOS was knocked down by siRNA and we found that knocking down SELENOS decreased TGF-β1 induced fibronectin expression. Our research indicates the potential value of ER-resident selenoproteins on renal fibrosis.

Keywords: Endoplasmic reticulum; HMCs; TGF-β1; glucose; selenoprotein N; selenoprotein S.

MeSH terms

  • Cells, Cultured
  • Endoplasmic Reticulum / metabolism*
  • Fibronectins / metabolism*
  • Glucose
  • Humans
  • Membrane Proteins / metabolism*
  • Mesangial Cells / metabolism*
  • Muscle Proteins / metabolism*
  • Selenoproteins / metabolism*
  • Transforming Growth Factor beta1

Substances

  • Fibronectins
  • Membrane Proteins
  • Muscle Proteins
  • SELENON protein, human
  • SELENOS protein, human
  • Selenoproteins
  • Transforming Growth Factor beta1
  • Glucose

Grants and funding

This work was supported by grants from the National Natural Science Foundation of China (81400740, 81470968, and 81300581).