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. Author manuscript; available in PMC: 2011 Aug 1.
Published in final edited form as: Glia. 2010 Aug;58(10):1177–1185. doi: 10.1002/glia.20997

Figure 5. Astrocyte-derived VEGF, controlled by HIF-2α, is a key mediator for neovascular tuft formation in OIR.

Figure 5

(A) In a murine model of oxygen-induced retinopathy (OIR), the area of vaso-obliteration induced by hyperoxia was quantified 24 hours after oxygen treatment (P13): there are no significant differences between GFAPcre+/VEGF+f/+f, GFAPcre+/HIF-1α+f/+f and GFAPcre+HIF-2α+f/+f animals and their respective wildtype littermates (data represents mean ± S.D.). (B,C) Gene expression analysis of VEGF (B) and EPO (C) in P13 retinae after hyperoxia shows that both genes are upregulated, indicating retinal hypoxia. However no genotype-specific difference of expression levels is observed between mice with conditional knockout of VEGF, HIF-1α and HIF-2α in astrocytes. (D-M) Vaso-obliteration and neovascular tuft formation in OIR was assessed at P17, 5 days after the end of the hyperoxic phase. (D-F) Loss of VEGF in astrocytes does not change vaso-obliteration but significantly reduces neovascularization. (G-I) Loss of HIF-1α in astrocytes does not affect vaso-obliteration or neovascularization in this OIR model, whereas (K-M) conditional deletion of HIF-2α significantly reduces vaso-obliteration and neovascularization relative to wildtype littermate controls (D,G,K: images show representative retina flatmounts (n>4 for all); E,F,H,I,L,M: data represents mean area relative to respective wildtype littermate controls ± S.D.).