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MDM2 phosphorylation mediates H2O2-induced lens epithelial cells apoptosis and age-related cataract

Zhongying Wang1, Dongmei Su2, Zhaoyi Sun3

  • 1Mudanjiang Medical College, Mudanjiang, 157011, Heilongjiang, China.

Biochemical and Biophysical Research Communications
|May 31, 2020
PubMed

Insights

MDM2 phosphorylation is crucial in preventing oxidative stress-induced apoptosis of lens epithelial cells, a key factor in age-related cataracts. This study reveals reduced MDM2 phosphorylation in cataracts, offering new therapeutic targets for ARC.

Area of Science:

  • Ophthalmology
  • Cell Biology
  • Molecular Medicine

Background:

  • Oxidative stress-induced apoptosis of lens epithelial cells (LECs) is a primary driver of age-related cataract (ARC) pathogenesis.
  • The precise molecular mechanisms underlying this process remain incompletely understood.

Purpose of the Study:

  • To investigate the role of MDM2 phosphorylation in ARC and hydrogen peroxide (H₂O₂)-induced LEC apoptosis.
  • To explore potential therapeutic strategies targeting MDM2 signaling pathways.

Main Methods:

  • Analysis of p-MDM2 levels in human cataractous and normal lens capsules.
  • Assessment of MDM2 phosphorylation in naturally aging cataract mouse models.
  • Construction of an oxidative stress-induced apoptosis model using HLE-B3 cells treated with H₂O₂.
  • Evaluation of MDM2 inhibitors and their effects on AKT signaling and apoptosis.

Main Results:

  • Reduced levels of phosphorylated MDM2 (p-MDM2 at Ser166 and Ser186) were observed in human cataracts and aging mouse models.
  • MDM2 was confirmed to regulate LEC apoptosis, with MDM2 inhibitors partially counteracting AKT's anti-apoptotic effect under H₂O₂ stress.
  • Decreased levels of phosphorylated AKT (p-AKT at Ser473) were noted in apoptotic LECs and ARC.

Conclusions:

  • MDM2 phosphorylation plays a significant role in mediating H₂O₂-induced LEC apoptosis and the development of ARC.
  • These findings suggest MDM2 signaling as a potential therapeutic target for clinical intervention in ARC.
Keywords:
Age-related cataractApoptosisLens epithelial cellsMDM2Phosphorylation

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