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. Author manuscript; available in PMC: 2020 Aug 3.
Published in final edited form as: Metabolism. 2019 Mar 19;95:27–35. doi: 10.1016/j.metabol.2019.03.004

Figure 4. SENP2 mediates leptin effects through the activation of PPARδ and PPARγ.

Figure 4.

(A) C2C12 myoblasts were transfected with mAcsl1(−1051)-Luc or mAcsl1(−1051)mt-Luc containing mutations at a potential PPRE (−210 bp), and then treated with leptin for 24 h. Luciferase activity of the cells, transfected with mAcsl1(−1051)-Luc without leptin, was expressed as 100, and the others were expressed as its relative values (n = 5). **P < 0.01. △, a PPRE site; ▲, a mutation at the PPRE site. (B) COS7 cells were transfected with one of PPAR expression vectors (100 ng), the SENP2 expression vector (100 ng), and mAcsl1(−1051)-Luc (300 ng) (n = 4). *P < 0.05, **P < 0.01 vs. PPARδ WT without SENP2, †P < 0.05, ††P < 0.01 vs. PAPRγ WT without SENP2. (C, D) C2C12 myotubes were treated with siNS or siSenp2 for 24 h, followed by treatment of leptin for another 24 h, and then ChIP was performed using PPARδ and PPARγ antibodies. Real time PCR was performed with the primers representing the flanking regions of the PPREs in the Acsl1 promoter (C) or Cpt1b promoter (D) (n = 4). *P < 0.05. Data are presented as mean ± SEM.