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
Figure 4. Notch-1 cKO in macrophages increased the SHP2 and suppressed the ROS in AAA. (A) DHE staining results showed the macrophages’ deficiency of Notch-1 suppressed the ROS production and its statistical data. N = 9; (B) macrophages’ deficiency of Notch-1 suppressed the expression of Notch-1, p22, p47 and consistent with increased expression of SHP2 in AAA tested by western blot. *P < 0.05, **P < 0.01, apoE-KO/Notch-1MAC-KO group vs. apoE-KO/Notch-1WT group.