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Fig. 1 | Molecular Neurodegeneration

Fig. 1

From: Targeting Hif1a rescues cone degeneration and prevents subretinal neovascularization in a model of chronic hypoxia

Fig. 1

Knockdown of Vhl in cones of the all-cone mouse (coneΔVhl). a Expression of Cre recombinase in BPCre;R91W;Nrl-/-;ZsGreen mice. Green fluorescence (ZsGreen) indicates Cre activity. RPE: retinal pigment epithelium, ONL: outer nuclear layer, INL: inner nuclear layer, IPL: inner plexiform layer, GCL: ganglion cell layer. Scale bar 50 μm. b PCR of genomic DNA from retinas of 4-week-old ctrl and coneΔVhl mice. Floxed Vhl (fl) is detected at 460 bp and Cre-mediated excision (ex) results in a 260 bp fragment. c Western blot analysis of HIF1A in 4, 6, 8 and 12-week-old coneΔVhl and ctrl (littermates without Cre recombinase) mice. ACTB served as loading control. d Relative expression of hypoxic target genes in retinas of ctrl (black) and coneΔVhl (orange) mice. Expression levels were normalized to beta-actin (Actb) and calculated relatively to 4-week-old ctrl mice, which were set to 1. Shown are means ± SD. Two-way ANOVA with Šídák’s multiple comparison test was used for statistical analysis (Adm: ****p<0.0001, *p=0.0306; Egln1: ****p<0.0001; Glut1: ****p<0.0001; Bnip3: ****p<0.0001, **p=0.0043; n≥3 per time point). Adm: Adrenomedullin, Egln1: egl-9 family hypoxia-inducible factor 1, Glut1: Glucose transporter 1, Bnip3: BCL2/adenovirus E1B interacting protein 3. Cre-negative littermates were used as ctrl mice in all experiments unless otherwise indicated

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