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EphA2 inhibits SRA01/04 cells apoptosis by suppressing autophagy via activating PI3K/Akt/mTOR pathway

Jing Han1, Lisong Wang1, Huayi Lv1

  • 1Department of Ophthalmology, Affiliated First Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, 230001, Anhui, China.

Archives of Biochemistry and Biophysics
|September 6, 2021
PubMed

Insights

EphA2 protein protects lens epithelial cells from hydrogen peroxide damage by inhibiting apoptosis and autophagy. This involves activating the PI3K/Akt/mTOR pathway, crucial for cell survival.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Ophthalmology

Background:

  • Oxidative stress, particularly from hydrogen peroxide (H2O2), is implicated in lens epithelial cell damage.
  • The role of EphA2 receptor tyrosine kinase in cellular responses to oxidative stress is not fully understood.

Purpose of the Study:

  • To investigate the effect of EphA2 on H2O2-treated lens epithelial cells (SRA01/04).
  • To elucidate the underlying molecular mechanisms, focusing on apoptosis, autophagy, and the PI3K/Akt/mTOR pathway.

Main Methods:

  • Cell viability and apoptosis assessed using MTT assay and flow cytometry.
  • Protein levels related to apoptosis and autophagy analyzed via Western blot.
  • Involvement of signaling pathways confirmed through specific inhibitors (MK-2206, Rapa).

Main Results:

  • EphA2 overexpression increased cell viability and decreased apoptosis in H2O2-treated cells.
  • EphA2 upregulated anti-apoptotic Bcl-2 and downregulated pro-apoptotic Cleaved-caspase-3 and Bax.
  • EphA2 suppressed autophagy and activated the PI3K/Akt/mTOR pathway (p-Akt, p-mTOR).

Conclusions:

  • EphA2 protects lens epithelial cells from H2O2-induced apoptosis by inhibiting autophagy.
  • The protective mechanism involves the activation of the PI3K/Akt/mTOR signaling pathway.
Keywords:
ApoptosisAutophagyEphA2PI3K/Akt/mTORSRA01/04 cells

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