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. Author manuscript; available in PMC: 2016 Apr 1.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2015 Feb 5;35(4):855–864. doi: 10.1161/ATVBAHA.114.304627

Fig. 4. The inhibition of Wnt signaling by VLN-NP in Vldlr−/− and OIR mice.

Fig. 4

A–D: Eyecups were isolated at P30 from LN-NP-treated WT (WT+LN), LN-NP-treated Vldlr−/− (VKO+LN) and VLN-NP-treated Vldlr−/− (VKO+VLN) group. Levels of proteins were measured by Western blot analysis (A). Each lane represents an individual animal. Densitometry was performed to semi-quantify p-LRP6 and t-LRP6 (B), n-p-β-catenin and t-β-catenin (C), and VEGF (D) which were normalized by β-actin levels. **p<0.01, *p<0.05, n=4. E–H: The retinas were dissected on P17 from LN-NP-treated Normoxia (N+LN), LN-NP-treated OIR (OIR+LN) and VLN-NP-treated OIR (OIR+VLN) groups. Levels of protein were measured by Western blot analysis (E). Densitometry was performed to semi-quantify p-LRP6 and t-LRP6 (F), n-p-β-catenin, t-β-catenin (G), and VEGF (H) levels, which were normalized by β-actin levels. **p<0.01, *p<0.05, n=3. I: X-gal staining of retinal sections: VLN-NP or LN-NP was injected intravitreally into BAT-gal mice (50 µg/eye) with OIR at P12. The retinas were dissected at P17 and sectioned, and β-galactosidase activities were evaluated by X-gal staining (blue). GCL: ganglion cell layer; INL: inner nuclear layer; ONL: outer nuclear layer; RPE: retinal pigment epithelium.