ArticleFrontiers in pharmacology2025
Prostaglandin E
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- The role of prostanoids in the retina and optic nerve in health and disease.Progress in retinal and eye research · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Introduction: Diabetic retinopathy (DR) is the leading cause of vision loss in working-age individuals globally, and the associated complication of diabetic macular edema (DME) is the most frequent cause of vision loss in these patients. The retinal swelling characteristic of DME can be attributed to fluid leakage due to damage to the two blood-retina barriers-the inner barrier composed primarily of retinal microvascular endothelial cells and the outer barrier composed of retinal pigment epithelial cells (RPE). Methods: Based on the previously characterized proinflammatory roles of prostanoid signaling in DR, we assayed the distinct prostanoid signaling mechanisms regulating inner and outer blood-retina barrier function using Results: Prostaglandin E2 (PGE2) stimulation of retinal endothelial monolayers caused a decrease in barrier permeability in electric cell-substrate impedance sensing (ECIS) assays and dextran flux assays. These effects occurred via the EP4 receptor of PGE2. In direct contrast, PGE2 stimulation of RPE monolayers caused an increase in barrier permeability via the EP2 receptor. Other prostanoids did not alter barrier permeability in either monocellular model. RNA sequencing of retinal endothelial and RPE cells with or without PGE2 stimulation revealed significant dysregulation of genes encoding junctional complex components and signaling that likely drive the observed effects on cell barrier resistance. Discussion: Together these results suggest opposing mechanisms of PGE2 signaling in the retina via two distinct receptors, indicating cell type-specific and likely receptor-specific targets for the potential therapeutic management of DME or other causes of dysfunctional retinal vascular permeability.
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Registered trials
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