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. 2013 Dec 19;2(6):e000548. doi: 10.1161/JAHA.113.000548

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© 2013 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.

This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

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Figure 6. — Hif2a deletion rescues the adipose tissue development and cardiac fibrosis in fatVHLko mice. A, Ratios of fat pad‐to‐body weight were analyzed using 1‐way ANOVA and post hoc Dunnett's multiple comparison test (n=17 for fatVHLwt, 8 for fatVHLko, 5 for fatVHL1Ako, 5 for fatVHL2Ako, and 7 for fatVHL1A2Ako). The white fat group (WAT) showed significant differences (P<0.001) especially with significant reduction of WAT in fatVHL1Ako mice compared with fatVHLwt. No differences were found in the BAT (interscapular fat) group. B, Angiogenesis was normalized in fatVHL2Ako and fatVHL1A2Ako, but not in fatVHL1Ako fat pads in comparison to fatVHLwt. B, Parafin‐embeded interscapular brown fat pads were stained with anti‐vWF and counterstained with hematoxylin. C, Cardiac fibrosis was analyzed using Masson's trichrome staining. Gross fibrosis (blue stain) was found in both fatVHLko and fatVHL1Ako hearts. Adipocyte deletion of Hif2a (fatVHL2A and fatVHL1A2A) was sufficient to rescue cardiac fibrosis. Scale bars=100 μm. BAT indicates brown adipose tissue; HIF, hypoxia‐inducible factor; KO, knockout; VHL, von Hippel–Lindau; vWF, von Willebrand factor; WAT, white adipose tissue; WT, wild type.