Comparative study of post-natal retinal vascular development in mice models of iPLA2 inhibition and plasmalogen deficiency

Purpose Plasmalogens are particular phospholipids characterized by the presence of a polyunsaturated fatty acid (PUFA) at sn-2 position of glycerol. Plasmalogen deficiency in mouse leads to developmental abnormalities in retinal vasculature. We propose that liberation of PUFA by the specific calcium-independent phospholipase A2 (iPLA2), is involved in the mechanism by which plasmalogens control retinal vascular development. To confirm this hypothesis, we performed a comparative study of retinal vascular development in a mouse model of retinal iPLA2 inhibition and a model of plasmalogen deficiency. Methods Vessel and astrocyte networks were visualized on flat-mounted retinas through immunostaining methods. Results Similar abnormalities were observed in retina of both mouse models. They consisted in an increased number of vessel ramifications at PN14, and in an abnormal glial cells migration from the optic nerve, at PN14 and at PN21. An activation of microglial cells was also observed at adult age. Conclusion These results confirm the implication of plasmalogen in the control of retinal vessel development through PUFA release from their sn-2 position.