Dysregulation of retinal vascularization is a common feature of several blinding diseases including retinopathy of prematurity, diabetic retinopathy and age-related macular degeneration. In DR and ROP, neovascular events occur at the level of retinal vessels and result in complications such as vitreous haemorrhages, torsional retinal detachment and subsequent blindness, whereas choroidal neovascularization is responsible for vision loss in patients with neovascular AMD. Since vascular development is tightly regulated by complex molecular interactions stimulating or inhibiting vasculogenesis and angiogenesis, the pathophysiological mechanisms involved in these diseases may include an imbalance between pro- and antiangiogenic compounds. Within the different factors influencing vascular growth, polyunsaturated fatty acids are drawing interest. In the retina, the major PUFAs are found primarily in neuronal and vascular cell membrane phospholipids from which they are released by phospholipases A2. Recent discoveries include in vitro data showing that PUFAs or their metabolites control the expression of pro-angiogenic growth factors in vascular cells, in vivo animal studies where dietary omega-3 PUFAs reduced pathological angiogenesis, and a large-scale human studies associating a higher dietary intake in omega-3 PUFAs with a slower progression of neovascular AMD. Not only PUFAs but also their phospholipid origin may be important in the control of vascular growth. Indeed, phospholipids in cell membranes can have different sub-types: conventional phospholipids on which fatty acids are connected through ester linkages or specific phospholipids termed “plasmalogens” where a vinyl–ether bond replaces an ester linkage. We have shown that plasmalogens accounts for 13% of retinal phospholipids and about 30% of retinal ethanolamine phospholipids. Given that plasmalogens are also considered to be reservoirs of PUFAs in membranes, they are suspected of having signalling functions by releasing these PUFAs through a specific calciumindependent PLA2. This hypothesis is reinforced by studies showing higher iPLA2 activities in various pathologic conditions involving Crizotinib plasmalogen metabolism. We speculated that a defective vessel maturation through pericyte recruitment would be involved in vessel dilation and tortuosity, and in the formation of vascular lesions. Because platelet-derived growth factor-beta signalling is required for pericyte recruitment and migration, we wanted to know whether the expression of pdgfb and pdgfrb genes is modified in the retinas of our mice model. Slight but significant down-regulation of pdgfb and pdgfrb genes was observed at PN21. However, immuno-stainings of retinal pericytes with anti-NG2 antibody did not reveal any impact of plasmalogen deficiency or iPLA2 inhibition on pericyte recruitment and positioning next to vessels, at any stage of development. Based on a preliminary description of the ocular phenotype of a mouse model of plasmalogen deficiency and to the wellknown implication of PUFAs in angiogenesis, we hypothesized that plasmalogens may participate in the control of retinal vascular development through PUFA release by a phospholipase belonging to iPLA2 family.