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Research Paper Volume 16, Issue 2 pp 1182—1191

Myeloid-specific knockout of Notch-1 inhibits MyD88- and TRIF-mediated TLR signaling pathways by regulating oxidative stress-SHP2 axis, thus restraining aneurysm progression

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Figure 3. Notch-1 cKO in macrophages promote the M2 polarization in AAA. (A) Immunofluorescence staining results showed the Notch-1 deficiency in macrophages inhibited the expression of iNOS (M1 marker) and increased the expression of arginase-1 (M2 marker) and statistical data; (B) macrophages’ deficiency of Notch-1 decreased the expression of iNOS and increased the expression of arginase-1 and IL-10 in AAA tested by western blot and the quantitative analysis. N = 6, *P < 0.05, **P < 0.01, apoE-KO/Notch-1MAC-KO group vs. apoE-KO/Notch-1WT group.