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Updated: Feb 6, 2026

Renal Ischaemia Reperfusion Injury: A Mouse Model of Injury and Regeneration
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Effect of long non-coding RNA growth arrest-specific 5 on apoptosis in renal ischaemia/reperfusion injury

Xuemei Geng1,2,3,4,5, Xialian Xu1,2,3,4,5, Yi Fang1,2,3,4,5

  • 1Department of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, China.

Nephrology (Carlton, Vic.)
|August 22, 2018
PubMed
Abstract

Insights

Long non-coding RNA GAS5 promotes kidney apoptosis during ischemia/reperfusion injury. This study investigated GAS5

Area of Science:

  • Molecular Biology
  • Renal Pathophysiology
  • RNA Biology

Background:

  • Long non-coding RNAs (lncRNAs) regulate critical cellular processes like apoptosis.
  • Renal ischemia/reperfusion (I/R) injury involves significant apoptosis.
  • The role of lncRNAs, specifically GAS5, in renal I/R injury-induced apoptosis remains underexplored.

Purpose of the Study:

  • To investigate the effect of hypoxia-responsive lncRNA growth arrest-specific 5 (GAS5) on apoptosis in renal I/R injury.
  • To elucidate the molecular mechanisms by which GAS5 influences apoptosis in kidney cells.

Main Methods:

  • Induction of renal I/R injury in mice and hypoxia/re-oxygenation (H/R) in human proximal renal tubular epithelial cells (HK-2).
  • Analysis of GAS5 mRNA and apoptosis-related gene (p53, cIAP2, TSP-1) expression at mRNA and protein levels.
  • Manipulation of GAS5 levels using small-interfering RNA (siRNA) and plasmid transfection in H/R-induced HK-2 cells.

Main Results:

  • Apoptotic cells were significantly increased in I/R-injured kidneys.
  • GAS5 expression was upregulated in response to I/R and H/R.
  • GAS5 upregulation correlated with increased p53 and cIAP2 levels.
  • GAS5 knockdown attenuated H/R-induced apoptosis and reduced p53 and TSP-1 expression.
  • GAS5 overexpression promoted apoptosis and increased p53 and TSP-1 expression in HK-2 cells.

Conclusions:

  • Long non-coding RNA GAS5, induced by I/R injury, promotes apoptosis in the kidney.
  • Thrombospondin-1 (TSP-1) may act as a downstream effector of GAS5 in mediating apoptosis.
  • Further research is warranted to fully explore the role of TSP-1 as a GAS5 downstream target.
Keywords:
acute kidney injuryapoptosisgrowth arrest-specific 5long non-coding RNA, renal ischaemia/reperfusion injury

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