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D-site binding protein regulates cell proliferation through mediating cell cycle progression in rat mesangial cells

Hongli Jiang1, Jie Li1, Xin He1

  • 1Dialysis Department of Nephrology Hospital, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, Shaanxi, China.

Tissue & Cell
|November 25, 2019
PubMed

Insights

D-site binding protein (DBP) prevents overproliferation of glomerular mesangial cells, a key factor in kidney damage. Reduced DBP levels correlate with increased cell proliferation in nephritis, suggesting DBP

Area of Science:

  • Nephrology
  • Molecular Biology
  • Cell Biology

Background:

  • Glomerular mesangial cell (MC) overproliferation disrupts kidney homeostasis, causing damage in mesangioproliferative glomerulonephritis.
  • Transcriptional factors are implicated in MC proliferation, but key regulators remain unidentified.

Purpose of the Study:

  • To identify the critical transcriptional factor inhibiting MC overproliferation.
  • To elucidate the regulatory mechanism of this factor in mesangial homeostasis.

Main Methods:

  • Microarray analysis of rat glomeruli with and without anti-Thy1 nephritis.
  • In vitro studies using primary rat MCs with DBP knockdown or overexpression.
  • EdU assays to measure cell proliferation capacity.
  • Analysis of cell cycle regulatory proteins (p21, p27, Cyclin D1).

Main Results:

  • D-site binding protein (DBP) was significantly decreased in rats with anti-Thy1 nephritis, correlating with MC overproliferation.
  • DBP knockdown promoted MC proliferation, while DBP overexpression inhibited it.
  • DBP arrested the G1/S phase transition by modulating p21, p27, and Cyclin D1 expression.

Conclusions:

  • DBP acts as a crucial inhibitor of MC proliferation by inducing G1 phase arrest.
  • Decreased DBP levels are a potential driver of mesangial overproliferation in anti-Thy1 nephritis.
  • DBP represents a potential therapeutic target for mesangioproliferative glomerulonephritis.
Keywords:
Cell proliferationD-site binding proteinGlomerulonephritis

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