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Vitamin E protects against retinopathy of prematurity through action on spindle cells
Insights
Vitamin E may reduce retinopathy of prematurity (ROP) severity by preventing abnormal blood vessel growth in premature infants. This study suggests a mechanism involving spindle cells and gap junctions, offering new insights into ROP prevention.
Area of Science:
- Ophthalmology
- Neonatology
- Developmental Biology
Background:
- Retinopathy of prematurity (ROP) is a blinding disease in premature infants.
- ROP incidence is increasing despite oxygen management, due to improved survival of very preterm infants.
- Vitamin E is known to be effective in suppressing severe ROP, but its mechanism is unclear.
Purpose of the Study:
- To propose a mechanism by which vitamin E protects against retinopathy of prematurity.
- To identify the role of spindle cells in ROP neovascularization.
- To investigate the effect of oxygen tension and vitamin E on spindle cell gap junctions.
Main Methods:
- The study proposes a mechanism involving spindle cells, the precursors of retinal capillaries.
- It investigates the effect of elevated oxygen tension on spindle cell gap junction area.
- It examines how vitamin E supplementation affects gap junction formation in infants with ROP.
Main Results:
- Elevated oxygen tension increases spindle cell gap junction area, halting normal vessel formation and triggering ROP neovascularization.
- Vitamin E supplementation suppresses gap junction formation in infants with low plasma vitamin E levels.
- Vitamin E reduces ROP severity but does not alter the overall incidence.
Conclusions:
- Spindle cells are proposed as key inducers of ROP neovascularization.
- Vitamin E's protective effect in ROP is mediated by suppressing oxygen-induced gap junction formation in spindle cells.
- This finding offers a potential mechanism for vitamin E's clinical efficacy in reducing ROP severity.
Abstract:
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.