Journal of Lipid Research · 9 authors, 2 centres
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Using neonatal physiological and pericyte-depletion-induced pathological retinal angiogenesis models in mice, the authors found that L-PGDS is required for normal physiological vessel elongation while H-PGDS restrains pathological angiogenesis and inflammation via DP1 signaling.
This preclinical study compared the roles of two prostaglandin D2 synthases, L-PGDS and H-PGDS, in murine retinal angiogenesis using two models: neonatal physiological angiogenesis (P8 retina) and pericyte-depletion-induced pathological angiogenesis (APB5 antibody-treated P8 retina). In the physiological model, L-PGDS-deficient mice showed reduced vessel elongation with excessive sprout formation and partial increases in VEGF, FGF-2, and EGF expression, while H-PGDS, DP1, and DP2 deficiencies had no effect. L-PGDS was expressed in endothelial and neural cells. In the pathological model, H-PGDS deficiency promoted hemorrhage and edema but inhibited the APB5-induced decrease in vessel elongation, whereas L-PGDS deficiency did not affect pathological angiogenesis. DP1 deficiency similarly inhibited the vessel elongation impairment. H-PGDS was expressed in infiltrated macrophages in the pathological retina. In vitro, L-PGDS inhibition increased hypoxia-induced VEGF expression in endothelial cells, which was suppressed by the PGD2 metabolite 15d-PGJ2. Vessel formation normalized by P14 even under L-PGDS deficiency.
