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Protecting vessel loss in the eyes of premature infants

As premature infants often have under-developed lungs, oxygen is administered following birth. One devastating side effect, however, is the development of retinopathy of prematurity (ROP), whereupon oxygen administration to the infant suppresses the expression of essential growth factors that promote the development of retinal blood vessels, resulting in blindness. In the July 1 issue of the Journal of Clinical Investigation, a study by researchers at Harvard Medical School and Children's Hospital, Boston investigating the development of the retinal vasculature in mice demonstrates that specific activation of the receptor VEGFR-1 by the growth factor PlGF-1 protects against oxygen-induced vessel loss.

ROP occurs in two distinct stages. First, exposure to high levels of oxygen causes obliteration of immature retinal vessels. The second phase, initiated upon return to breathing normal air, results in an adverse overcompensation of new vessel growth. The new vessels are excessive in number and often leaky. The inner membrane of the retina can be breached, whereby vessels grow into the vitreous of the eye causing retinal detachment and blindness.

The process of vasculature development is mediated in part by the growth factor VEGF. It had been shown previously that vessels can be rescued by administration of VEGF, suggesting that VEGF might be used in the treatment of ROP. However, this theory presents a double-edged sword as VEGF also stimulates abnormal vessel growth that can ultimately result in leaky vessels.

In order to wisely skirt this catastrophic event, Lois E. H. Smith and colleagues utilized placental growth factor-1 (PlGF-1), which exclusively activates the VEGF receptor-1 (VEGFR-1). The authors demonstrate that the administration of PlGF-1 protects against oxygen-induced vessel loss without provoking neovascularization. Unlike VEGF, which interacts with both forms of the VEGF receptor (VEGFR-1 and VEGFR-2), PlGF-1 only binds VEGFR-1.
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Contact: Brooke Grindlinger
science_editor@the-jci.org
212-342-9006
Journal of Clinical Investigation
1-Jul-2003


Page: 1 2

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