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Figure 3 | Acta Neuropathologica Communications

Figure 3

From: Critical role of TNF-alpha-TNFR1 signaling in intracranial aneurysm formation

Figure 3

Suppression of inflammatory responses in IA walls resulting from defective TNFR1 signaling. (A) Immunohistochemistry to detect the phosphorylated form of the NF-kappaB p65 subunit (p-p65) in IA walls located at right anterior cerebral artery-olfactory artery bifurcations in wild-type and TNFR1-deficient (TNFR1 KO) mice. Immunohistochemistry for anti- smooth muscle alpha actin (SMA) was used to indicate the media of IA walls. Bar = 50 um. (B) Immunohistochemistry for COX-2 (upper columns), or MCP-1 (lower columns), and SMA (red color) in IA walls of wild-type and TNFR1 KO mice. Bar = 50 um. In the right panels, the relative intensities of positive signals of COX-2 and MCP-1 in IA walls from the left panels are shown. The number of mice used is shown in parentheses. *indicates p < 0.05. All bars indicate the mean ± SEM. (C) mRNA expression of COX-2 and MCP-1 in wild-type and TNFR1 KO mice from quantitative real-time (qRT)-PCR analysis. n = 4 for wild-type and 3 for TNFR1 KO mice. *indicates p < 0.05. All bars indicate the mean ± SEM. (D) The number of macrophages, F4/80-positive cells, in IA walls of wild-type and TNFR1 KO mice. All bars indicate the mean ± SEM. The number of mice used is shown in parentheses. *indicates p = 0.0061.

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