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. 2016 Feb 18;6:21382. doi: 10.1038/srep21382

Figure 5. PPARγ inhibits adipose oxidative stress and inflammation by interacting directly with Mark4.

Figure 5

(A) Fragments of Mark4 promoter fused to a luciferase reporter gene were co-transfected into cells together with PGL3-basic (control) or pc-PPARγ (n = 3). Luciferase activity was corrected for Renilla luciferase activity and normalized to control activity (n = 3). (B) Relative mRNA expression of Mark4 and PPARγ of the primary adipocytes incubated for 24 h in the presence of 100 nM rosiglitazone (n = 3). (C) Relative mRNA expression of Mark4 and PPARγ of the primary adipocytes with pc-PPARγ transfected for 48 h (n = 3). (D) Mark4 interacted with PPARγ. Immunoprecipitation (IP) analysis was performed in HA-Mark4 and pc-PPARγ transfected cells (n = 3). (E) ChIP analysis of Mark4 and PPARγ in adipocytes (n = 3). (F) Relative activity of ROS and SOD after transfection with HA-Mark4 and pc-PPARγ for 48 h in primary adipocyte (n = 3). (G) Relative mRNA of leptin and IL-6 after transfection with HA-Mark4 and pc-PPARγ for 48 h in primary adipocyte (n = 3). Control: transfection of pcDNA3.1-vector group, HA-Mark4 group: overexpression of Mark4 group, pc-PPARγ: overexpression of PPARγ group. Values are means ± SD. vs. control group, *p < 0.05.