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Adenosine triphosphate-induced rabbit corneal endothelial cell proliferation in vitro via the P2Y2-PI3K/Akt signaling

Junzhao Chen1, Chunyi Shao, Wenjuan Lu

  • 1Department of Ophthalmology, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, PR China.

Cells, Tissues, Organs
|October 18, 2014
PubMed
Abstract

Insights

Adenosine triphosphate (ATP) at 10 μM significantly enhances rabbit corneal endothelial cell (RCEC) proliferation. This effect is mediated through the P2Y2 receptor and the PI3K/Akt signaling pathway, crucial for cell growth.

Area of Science:

  • Ophthalmology
  • Cell Biology
  • Molecular Signaling

Background:

  • Rabbit corneal endothelial cells (RCECs) are vital for maintaining corneal transparency.
  • Understanding factors that promote RCEC proliferation is crucial for regenerative medicine and treating corneal diseases.
  • The adenosine triphosphate (ATP)-P2Y2 receptor signaling pathway is implicated in various cellular processes.

Purpose of the Study:

  • To investigate the role of the ATP-P2Y2-PI3K/Akt signaling axis in promoting RCEC proliferation in vitro.
  • To determine the optimal concentration of ATP for stimulating RCEC growth.
  • To elucidate the specific molecular mechanisms involved in ATP-induced RCEC proliferation.

Main Methods:

  • RCECs were treated with varying concentrations of ATP (1-100 μM).
  • Cell proliferation was assessed using Cell Counting Kit-8 (CCK8) and Ki67 staining.
  • P2Y2 receptor agonists/antagonists and PI3K/Akt inhibitors were used to evaluate pathway involvement.
  • Western blotting analyzed Akt phosphorylation levels in response to ATP and inhibitors.

Main Results:

  • 10 μM ATP significantly promoted RCEC proliferation; 25 μM showed a lesser effect.
  • P2Y2 receptor agonists mimicked ATP's proliferative effect, while antagonists blocked it.
  • ATP induced Akt phosphorylation, which was inhibited by P2Y2 antagonists and PI3K/Akt inhibitors.
  • The proliferative effect of ATP was dependent on the P2Y2-PI3K/Akt pathway.

Conclusions:

  • 10 μM ATP markedly promotes rabbit corneal endothelial cell proliferation.
  • The P2Y2-PI3K/Akt signaling axis is essential for ATP-induced RCEC proliferation.
  • This pathway represents a potential therapeutic target for enhancing corneal endothelial wound healing.

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