Figure 6.

Activation 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% O₂ 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.