Selective stimulation of VEGFR-1 prevents oxygen-induced retinal vascular degeneration in retinopathy of prematurity
J. Clin. Invest. Shu-Ching Shih, et al. 112:50 doi:10.1172/JCI17808 [
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Figure 6Activation of VEGFR-1 by PlGF-1 does not increase normal retinal vessel growth or revascularization. (
a) Intravitreal injections at P3 of control (BSS) in one eye and PlGF-1 in the contralateral eye (
n = 6). Retinal vessel growth area was measured in whole mounts at P5. PlGF-1–injected eyes had a mean of 41.67% ± 5.63% of the retina vascularized. Similarly, 42.18% ± 8.60% of the BSS-injected contralateral control eyes were vascularized (
P = 0.91). Results are representative of two independent experiments. (
b) Vessel revascularization was measured in P15 mice after induction of vessel loss by oxygen (P7–P12) followed by intravitreal injections of BSS at P13 in one eye and PlGF-1 in the contralateral eye. PlGF-1–injected eyes were 26.32% ± 2.62% vascularized; similarly, BSS-treated contralateral control eyes were 26.29% ± 2.86% vascularized (
n = 6,
P = 0.99). Results are representative of two independent experiments. (
c) In eyes with oxygen-induced retinopathy, the mean number of vascular nuclei extending into the vitreous at P17 in ten retinal cross sections per eye (
n = 8 eyes) was counted after intravitreal injections of BSS at P13 (after 5 days of 75% O
2 treatment, from P7 to P12) in one eye and PlGF-1 in the contralateral eye. BSS- and PlGF-1–injected eyes showed means of 9.98 and 9.96 vascular nuclei (
P = 0.61), respectively, indicating no stimulation of proliferation by PlGF-1.