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. Author manuscript; available in PMC: 2011 May 29.
Published in final edited form as: Nature. 2008 Nov 9;456(7223):814–818. doi: 10.1038/nature07445

Figure 2.

Figure 2

Deletion of VEGF in myeloid cells leads to a normalized vasculature and higher tumor volumes in Lewis Lung Carcinoma isografts.

a, Growth curve analysis of Lewis Lung Carcinoma (LLC) tumors injected subcutaneously in WT and Mut mice (n>7 for each group). b, Quantitative analysis of CD 31-positive endothelial cells (n=4). c, Determination of blood vessel tortuosity in LLC tumors. d, Left: Immunoblotting for VEGFR2 and phosphotyrosine (p-Tyr) after Immunoprecipitation of VEGFR2 from LLC tumor lysates. Center: Quantitative analysis of VEGFR2 (upper) and phosphotyrosine (lower) signals. Right: Ratio of p-Tyr and VEGFR2 signal intensities as a measure of receptor activation (WT n=8, Mut n=7). e, Left: Confocal microscopy images of simultaneous immunodetection of endothelial cells and pericytes in LLC tumors with the specific markers CD 31 and smooth muscle actin-alpha (SMA-alpha). Right: Pericyte coverage as assessed by SMA-alpha/CD 31 co-localization (n=4). f, Left: Fluorescent microscopy images of a FITC-dextran angiography on LLC isografts. Right: Ratio of extravascular over intravascular FITC-dextran as a measure of vascular permeability (WT n=6, Mut n=4). Scale bar, 100 μm; error bars, s.e.m.