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Response gene to complement 32 regulates the G2/M phase checkpoint during renal tubular epithelial cell repair

Yun-Lin Shen1, Hua-Jie Liu1, Lei Sun1

  • 1Department of Nephrology and Rheumatology, Shanghai Children's Hospital, Shanghai Jiao Tong University, Shanghai, 200062 China.

Cellular & Molecular Biology Letters
|May 25, 2017
PubMed
Abstract

Insights

Response gene to complement 32 (RGC-32) influences renal tubular epithelial cell repair by regulating cell cycle and fibrosis. Silencing RGC-32 induced G2/M arrest and promoted fibrosis, impacting cell adhesion.

Area of Science:

  • Nephrology
  • Cell Biology
  • Molecular Medicine

Background:

  • Renal tubular epithelial cell injury is a critical factor in kidney disease progression.
  • Response gene to complement 32 (RGC-32) is implicated in cellular stress responses.
  • The role of RGC-32 in renal tubular cell cycle regulation and injury repair remains unclear.

Purpose of the Study:

  • To investigate the influence of RGC-32 on cell cycle progression in renal tubular epithelial cells during injury.
  • To assess the impact of RGC-32 modulation on fibrosis markers and cell adhesion.

Main Methods:

  • NRK-52E cells were manipulated for RGC-32 overexpression or silencing using plasmid transfection.
  • Cell cycle distribution was analyzed using flow cytometry.
  • Expression of fibrosis markers (α-SMA, FN, E-cadherin) and NGAL was evaluated via qPCR or Western blot.

Main Results:

  • TNF-α treatment induced renal tubular epithelial cell injury, marked by increased NGAL and RGC-32 expression.
  • RGC-32 silencing led to G2/M cell cycle arrest.
  • Silencing RGC-32 significantly increased α-SMA and FN expression while decreasing E-cadherin, indicating enhanced fibrosis and reduced cell adhesion.

Conclusions:

  • RGC-32 plays a significant role in the repair of renal tubular epithelial cells in vitro.
  • RGC-32 regulates the G2/M phase checkpoint, thereby influencing cell cycle progression.
  • RGC-32 impacts cell fibrosis and adhesion, suggesting a potential therapeutic target for kidney injury.
Keywords:
Cell cycleG2/M phaseResponse gene to complement 32Tubular epithelial cell repairTubulointerstitial fibrosisTumor necrosis factor-alpha

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