1.25(OH)2D3 decreases PCNA and mTOR expression and alleviates renal injury in Thy-1 nephritis rat model

Jian-Feng Li1, Lei Jin2, Huan Ma3

  • 1Department of Nephrology, The First People's Hospital of Nanyang City, Nanyang, Henan Province, China.

Plos One
|December 5, 2024
PubMed
Abstract

Insights

This study shows that 1.25(OH)2D3 significantly reduces mesangial cell proliferation in proliferative glomerulonephritis. It also reveals the involvement of mTOR protein in this process, clarifying how 1.25(OH)2D3 alleviates renal injury.

Area of Science:

  • Nephrology
  • Endocrinology
  • Molecular Biology

Background:

  • Proliferative glomerulonephritis is characterized by mesangial cell proliferation.
  • 1.25(OH)2D3 is a vitamin D metabolite with potential therapeutic roles.

Purpose of the Study:

  • To investigate the role and mechanisms of 1.25(OH)2D3 in proliferative glomerulonephritis.
  • To determine its effect on mesangial cell regulation.

Main Methods:

  • A rat model of proliferative glomerulonephritis was established.
  • Rats were treated with 1.25(OH)2D3 and/or rapamycin.
  • Renal injury, mesangial cell proliferation (PCNA), and mTOR expression were assessed.

Main Results:

  • 1.25(OH)2D3 significantly reduced mesangial cell proliferation and PCNA expression.
  • mTOR expression was increased in nephritis and reduced by 1.25(OH)2D3 treatment.
  • These effects were observed across multiple time points post-intervention.

Conclusions:

  • 1.25(OH)2D3 effectively inhibits glomerular mesangial cell proliferation in glomerulonephritis.
  • The mammalian target of rapamycin (mTOR) pathway is implicated in the mechanism of action of 1.25(OH)2D3.
  • These findings highlight 1.25(OH)2D3 as a potential therapeutic agent for glomerulonephritis.