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. Author manuscript; available in PMC: 2014 Apr 1.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2013 Feb 14;33(4):795–804. doi: 10.1161/ATVBAHA.113.301220

Figure 4. AIP1 deletion increases plaque and systemic inflammatory responses.

Figure 4

ApoE−/− and DKO adult mice were fed with chow or Western-type diet for 10 weeks. A. Effects of AIP1 deletion on proinflammatory cytokine production. TNF, IL-6, IL-12 and IL-10 in plasma were measured by ELISA. Data are presented are mean±SEM, n=8 mice in each group. B. Inflammatory responses in the plaques. NF-κB and JNK signaling in atherosclerotic plaques were measured by immunoblotting with phospho-p65- and p-JNK-specific antibodies. Total AIP1 and β-actin proteins were also determined. N=3 mice per group C. Enhanced NF-κB signaling and ICAM-1 expression in DKO vascular endothelium. NF-κB activity and ICAM-1 expression in brachiocephalic arteries lesions from ApoE−/− and DKO mice were stained with anti-p-P65 and anti-ICAM-1. CD31 was used for EC staining. Representative images are shown in panel C. Scale bar: 50 μm. Macrophages within the endothelium layer and the plaque were quantified in D. Data are mean±SEM from 6 mice per group. *, p<0.05. E. Transcripts for macrophage recruitment chemokines MCP-1, Rantes and CX3CL1 were quantified by qRT-PCR and normalized to hypoxanthine guanine phosphoribosyltransferase (HPRT) from ApoE and DKO aortas. Data are mean±SEM from 5 mice per group. *, p<0.05.