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microRNA-183 Mediates Protective Postconditioning of the Liver by Repressing Apaf-1

Han-Chen Lin1,2, Shin-Yun Liu1, Er-Yen Yen1

  • 11 Department of Anatomy and Cell Biology, Medical College, National Taiwan University , Taipei, Taiwan .

Antioxidants & Redox Signaling
|September 1, 2016
PubMed
Abstract

Insights

Ischemic postconditioning protects the liver from reperfusion injury by upregulating microRNA-183 (miR-183). This microRNA targets apoptosis signaling, reducing liver damage and promoting cell survival.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cell Biology

Background:

  • Ischemic postconditioning (iPoC) is a protective intervention against ischemia-reperfusion (IR) injury.
  • The precise molecular mechanisms underlying iPoC's protective effects on the liver are not fully understood.

Purpose of the Study:

  • To investigate the role of microRNA-183 (miR-183) in the protective mechanism of iPoC in liver IR injury.
  • To elucidate the signaling pathway through which miR-183 exerts its protective effects.

Main Methods:

  • In vitro studies using an oxygen-glucose deprivation (OGD) model in Clone 9 cells with hypoxic postconditioning (HPoC) and miR-183 modulators (mimetic and inhibitor).
  • In vivo studies in mice subjected to liver IR injury, treated with iPoC and miR-183 modulators (agomiR-183 and antagomiR-183).
  • Analysis of cell death, apoptosis-related protein expression (Apaf-1, caspase-3/9), and liver injury markers (ALT, 4-HNE) using biochemical assays and histological staining (H&E, TUNEL).

Main Results:

  • miR-183 expression was significantly increased by iPoC in rat livers.
  • miR-183 repressed Apaf-1 mRNA expression, a key factor in apoptosis.
  • In vitro, HPoC and miR-183 mimetics reduced cell death and apoptosis signaling (Apaf-1, caspase-3/9) after OGD, effects abolished by miR-183 inhibitors.
  • In vivo, iPoC and agomiR-183 reduced liver injury markers (ALT) and apoptosis (Apaf-1, 4-HNE) post-IR, while antagomiR-183 diminished iPoC's protective effects.

Conclusions:

  • miR-183 is a critical mediator of the protective effects of iPoC in liver IR injury.
  • miR-183 confers tolerance to IR injury by repressing the apoptotic signaling pathway through targeting Apaf-1.
  • This study reveals a novel mechanism by which miR-183 contributes to liver protection during postconditioning.
Keywords:
hypoxic postconditioningmiR-183oxygen-glucose deprivation

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