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Updated: Jun 13, 2026

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation
Published on: May 23, 2025
Role of platelet-activating factor in cell death signaling in the cornea: A review
Salomon Esquenazi1, Haydee E P Bazan
1Neuroscience Center of Excellence and Department of Ophthalmology, LSU Health Sciences Center, New Orleans, LA, USA.
Abstract:
Platelet-activating factor (PAF) is a potent bioactive lipid generated in the cornea after injury whose actions are mediated through specific receptors. Studies from our laboratory have shown that PAF interactions with its receptors activate several transmembrane signals involved in apoptosis. Continuous exposure to PAF during prolonged inflammation increases keratocyte apoptosis and inhibition of epithelial adhesion to the basement membrane. As a consequence, there is a marked delay in wound healing, which is not countered by the action of growth factors. While apoptosis of stroma cells is rapid and potent, epithelial cells as well as myofibroblasts, which appear in the stroma during the repair phase, are resistant to apoptosis. However, PAF accelerates apoptosis of corneal epithelial cells exposed to oxidative stress by stimulating phospholipase A2, producing an early release of cytochrome C from mitochondria and activating caspase-3. In myofibroblasts, PAF has a synergistic action with tumor necrosis factor-alpha (TNF-alpha), increasing apoptosis of the cells to 85%. PAF antagonists block the effects of PAF and could have a therapeutic role in maintaining a healthy and transparent cornea.
Insights
Platelet-activating factor (PAF) promotes corneal cell death and delays wound healing. PAF antagonists may protect the cornea by blocking these effects, preserving transparency.
Area of Science:
- Ophthalmology
- Cell Biology
- Wound Healing Research
Background:
- Platelet-activating factor (PAF) is a lipid mediator released in the cornea post-injury.
- PAF signaling through its receptors triggers transmembrane signals linked to apoptosis.
- Prolonged PAF exposure during inflammation impairs corneal wound healing.
Purpose of the Study:
- To investigate the role of PAF in corneal cell apoptosis and wound healing.
- To determine the mechanisms by which PAF affects corneal epithelial cells and myofibroblasts.
- To evaluate the therapeutic potential of PAF antagonists in corneal repair.
Main Methods:
- Analysis of PAF-induced apoptosis in corneal cells (keratocytes, epithelial cells, myofibroblasts).
- Investigation of PAF's interaction with phospholipase A2, mitochondria, and caspase-3 activation.
- Assessment of PAF's synergistic effects with TNF-alpha in myofibroblast apoptosis.
- Evaluation of PAF antagonist efficacy in blocking PAF-mediated effects.
Main Results:
- Continuous PAF exposure causes keratocyte apoptosis and inhibits epithelial adhesion, delaying wound healing.
- Corneal epithelial cells and myofibroblasts show differential resistance to PAF-induced apoptosis.
- PAF accelerates apoptosis in epithelial cells under oxidative stress via phospholipase A2, cytochrome C, and caspase-3.
- PAF synergizes with TNF-alpha to induce significant apoptosis (85%) in myofibroblasts.
Conclusions:
- PAF plays a critical role in corneal inflammation-induced apoptosis and delayed wound healing.
- PAF antagonists offer a potential therapeutic strategy for maintaining corneal transparency and health.
- Targeting PAF signaling could be beneficial in managing corneal injuries and inflammatory conditions.
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