MED1 Deficiency in Macrophages Accelerates Intimal Hyperplasia via ROS Generation and Inflammation

Figure 6

MED1 deficiency enhances NF-κB and STAT1 activation in macrophages. (a) qRT-PCR analysis of TNFα and iNOS levels in MED1^fl/fl and MED1^ΔMac macrophages treated with Bay11-7082 and LPS. (b) qRT-PCR analysis of p65, STAT1, STAT3, and Jun levels in MED1^fl/fl and MED1^ΔMac macrophages treated with LPS for 6 h. (c) Western blotting analysis of levels of phosphorylated NF-κB p65 in peritoneal macrophages treated with LPS for 6 h. (d) Quantitative analysis of levels of phosphorylated NF-κB p65. (e) Western blotting analysis of levels of phosphorylated STAT1 in peritoneal macrophages treated with LPS for 6 h. (f) Quantitative analysis of levels of phosphorylated STAT1. (g, h) MED1^fl/fl and MED1^ΔMac macrophages treated with or without Bay11-7082 before LPS incubation; the culture medium of macrophages was collected and centrifuged to remove suspended cells for subsequent experiments. (g) Migration of smooth muscle cells was determined by wound healing after adding macrophage medium for 24 h. (h) The proliferation of smooth muscle cells was measured by CCK8 after adding macrophage medium for 24 h (–6). The data are expressed as the . .

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