Vitamin E protects against retinopathy of prematurity through action on spindle cells.
In the premature infant, exposure of the incompletely vascularized retina to increased oxygen tension can result in the development of a blinding disease, retinopathy of prematurity (ROP). Despite the judicious curtailment of oxygen, the incidence of ROP is on the increase due to the technological advances that have improved the survival of the very young preterm infant. Six clinical trials have documented the efficacy of vitamin E supplementation in suppressing the development of severe ROP, but the mechanism of this protection has remained unknown. This report proposes that spindle cells, mesenchymal precursors of the inner retinal capillaries, are the primary inducers of the neovascularization associated with ROP. Exposure of spindle cells to elevated oxygen tension increases their gap junction area. This early morphologic event immediately halts the normal vasoformative process and eventually triggers the neovascularization that is observed clinically 8-12 weeks later. Vitamin E supplementation above the deficient plasma levels of these infants suppresses gap junction formation and clinically reduces the severity without altering the total incidence of ROP.
D006801:Humans; D007231:Infant, Newborn; D007234:Infant, Premature; D008854:Microscopy, Electron; D012160:Retina / Q000473:pathology* / Q000648:ultrastructure; D012164:Retinal Diseases / Q000151:congenital* / Q000473:pathology / Q000517:prevention & control; D014810:Vitamin E / Q000627:therapeutic use*
D014810:Vitamin E