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. Author manuscript; available in PMC: 2017 Feb 1.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2015 Dec 3;36(2):350–360. doi: 10.1161/ATVBAHA.115.306713

Figure 2. LRP1 deletion in retinal endothelium displays increased proliferation without changes in the interaction of endothelial cells with astrocytes and pericytes.

Figure 2

A–B, Endothelial cell proliferation increases in LRP1f/f;Cre+ mice. (A) Retinal sagittal sections from P15 (72 hours of hypoxia) LRP1f/f;Cre+/− mice were stained with Ki67 (cell proliferation marker, green), CD31 (endothelial cell marker, red) and DAPI (blue). The percentage of Ki67 positive endothelial cells were counted and presented in B. Arrows, Ki67 positive endothelial cells. *, P<0.05 via unpaired Student’s t-test, n=6 for LRP1f/f;Cre− and n=5 for LRP1f/f;Cre+ mice. C–D, Normal astrocyte-endothelial filopodia interactions and pericyte recruitment are observed in both LRP1f/f;Cre+ and LRP1f/f;Cre− mouse retinas. Flat-mounted whole retinas from LRP1f/f;Cre+/− mice that were subjected to OIR for 48 hours were stained with iso-lectin (red), glial fibrillary acidic protein (GFAP; green in C) or NG2 (green in D). Arrows, endothelial filopodia.