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. 2014 Dec 29;9(12):e115974. doi: 10.1371/journal.pone.0115974

Figure 7. Knockout of PHD2 reduces HFD-induced NF-κb activation and macrophage infiltration in HFD mice.

Figure 7

(A) NF-κb expression was significantly decreased in the hearts of PHD2KO+HFD mice compared to WT, Cre+ + HFD mice at 16 weeks (n = 4 mice, *p<0.05). (B) TLR4 expression was significantly reduced in the hearts of PHD2KO+HFD mice compared to WT, Cre+ + HFD mice at 16 weeks (n = 4–5 mice, *p<0.05). (C) MyD88 expression was significantly suppressed in the hearts of PHD2KO+HFD mice compared to WT, Cre+ + HFD mice at 16 weeks (n = 4–5 mice, *p<0.05). (D) IRAK-4 expression was significantly inhibited in the hearts of PHD2KO+HFD mice compared to WT, Cre+ + HFD mice at 16 weeks (n = 4 mice, *p<0.05). (E and F) The expression of ICAM-1 and TNF-α was significantly reduced in the hearts of PHD2KO+HFD mice compared to WT, Cre+ + HFD mice at 16 weeks (n = 6 mice, *p<0.05). (G and H) Inflammatory cell infiltrations were stained with macrophage markers CD45 (green) and CD11b (Red). Nuclei were counterstained with DAPI (blue). Immunohistochemical analysis of macrophage infiltrations (CD45 and CD11b positive cells) showing the number of macrophage (white arrow) was increased in the hearts of WT, Cre+ + HFD mice compared to that of WT, Cre+ + ND mice. Knockout of PHD2 dramatic reduced the number of macrophage in the hearts of HFD mice.