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. 2016 Aug 5;7:12152. doi: 10.1038/ncomms12152

Figure 3. Effects of VEGF and VEGFR blockades on CL-induced adipose angiogenesis and beige phenotype.

Figure 3

(a) Microvessels (CD31+ red), adipocyte morphology (H&E; perilipin+ green) and UCP1 expression (UCP1+ red) of CL-treated gWAT in mice that were treated with vehicle, VEGF-, and VEGFR2-specific neutralizing antibodies (Anti-VEGF and Anti-R2) and sunitinib. The vehicle- treated group served as a control. White arrows and arrowheads in upper three panels point to microvessels. Arrows in the lowest row of panels indicate UCP1-positive signals. Double-arrowed bars mark adipocyte diameter. Green=perilipin; blue=DAPI. n=8 for each vehicle, VEGF and VEGFR blockades group. (b) Quantification of microvessel density in vehicle- and CL-treated wt mice that received treatment with various VEGF blockades (n=10 random fields; n=8 mice for each group). (c) Quantification of average adipocyte size (>30 adipocytes/field; n=10 random fields; n=8 mice for each group). (d) Quantification of UCP1-positive signals (n=10 random fields; n=8 mice for each group). (e) Norepinephrine-stimulated non-shivering thermogenesis in VEGF/VEGFR blockade- and vehicle-treated mice that received CL or buffer (n=5 mice for each group). All scale bars, 50 μm. *P<0.05; **P<0.01; ***P<0.001 by two-sided unpaired t-test. Data presented as mean±s.e.m. NE, norepinephrine.