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. 2015 Aug 20;19(12):2715–2727. doi: 10.1111/jcmm.12657

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© 2015 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.

This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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Nlrp3 deficiency gene deletion inhibits high‐fat diet (HFD)‐induced inflammasome activation in mouse coronary arterial endothelium. Wild‐type (Nlrp3^+/+) or Nlrp3 knockout (Nlrp3^−/−) Mice were fed with normal diet (ND) and high‐fat diet (HFD) for 6 weeks. Frozen sections of mouse hearts were stained with FLICA, a green fluorescent probe specific for active caspase‐1, and Alexa555‐conjugated antibodies against an endothelium marker vWF in coronary arteries. (A) The merged images displayed yellow dots or patches indicating the colocalization of FLICA (green) with vWF (red). Enlarged images of area of interest (AOI) in merged images are shown; scale bar = 50 μm. (B) The summarized data show the colocalization coefficient of FLICA with vWF (n = 5–7). *P < 0.05 versus Nlrp3 ^+/+ with ND; ^# P < 0.05 versus Nlrp3 ^+/+ with HFD.