Abstract
ObjectiveProper development of retinal blood vessels is essential to ensure sufficient oxygen and nutrient supplies to the retina. It was shown that polyunsaturated fatty acids (PUFAs) could modulate factors involved in tissue vascularization. A congenital deficiency in ether-phospholipids, also termed “plasmalogens”, was shown to lead to abnormal ocular vascularization. Because plasmalogens are considered to be reservoirs of PUFAs, we wished to improve our understanding of the mechanisms by which plasmalogens regulate retinal vascular development and whether the release of PUFAs by calcium-independent phospholipase A2 (iPLA2) could be involved.Methods and ResultsBy characterizing the cellular and molecular steps of retinal vascular development in a mouse model of plasmalogen deficiency, we demonstrated that plasmalogens modulate angiogenic processes during the early phases of retinal vascularization. They influence glial activity and primary astrocyte template formation, endothelial cell proliferation and retinal vessel outgrowth, and impact the expression of the genes involved in angiogenesis in the retina. These early defects led to a disorganized and dysfunctional retinal vascular network at adult age. By comparing these data to those obtained on a mouse model of retinal iPLA2 inhibition, we suggest that these processes may be mediated by PUFAs released from plasmalogens and further signalling through the angiopoietin/tie pathways.ConclusionsThese data suggest that plasmalogens play a crucial role in retinal vascularization processes.
Highlights
Vascular growth occurs through two complementary mechanisms: vasculogenesis and angiogenesis [1]
They influence glial activity and primary astrocyte template formation, endothelial cell proliferation and retinal vessel outgrowth, and impact the expression of the genes involved in angiogenesis in the retina
These early defects led to a disorganized and dysfunctional retinal vascular network at adult age. By comparing these data to those obtained on a mouse model of retinal independent phospholipase A2 (iPLA2) inhibition, we suggest that these processes may be mediated by polyunsaturated fatty acids (PUFAs) released from plasmalogens and further signalling through the angiopoietin/tie pathways
Summary
Vascular growth occurs through two complementary mechanisms: vasculogenesis and angiogenesis [1]. Vasculogenesis corresponds to the initial vascular tree formation by differentiation of vascular endothelial lineage precursor cells, whereas fine endothelial cell extensions arise by sprouting from pre-existing vessels during angiogenesis. Whereas all vascular laminae emerge post-natally in several mammal species, the innermost plexus arises at gestational age in humans, while the deeper vascular laminae are formed at around 24 weeks of gestation and continue developing after birth [2]. Nutrients are supplied to the anterior eye by hyaloid vessels extending from the optic disc. The development of the retinal vasculature coincides with hyaloid vasculature regression [3]. The hyaloid vascular system fully regresses before birth in humans and during the first post-natal weeks in mice
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