Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2013 Feb 14;62(3):762–774. doi: 10.2337/db12-0570

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2013 by the American Diabetes Association.

Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.

PMC Copyright notice

FIG. 1. — Effect of TM on PPARδ expression and activity in C2C12 myotubes. A: PPRE activity in C2C12 myotubes transfected with pTK-PPREx3-luc was evaluated by luciferase assay. PPARδ expression in C2C12 myotubes transfected with pTK-PPREx3-luc was detected by Western blotting. C2C12 myotubes with cotransfection the plasmid pAdTrack-CMV-PPAR-δ, containing the full-length coding region of rat PPARδ (PPARδ vector), were treated with DMSO (control [CON]) or TM (10 μmol/L) for 15 min to 24 h before the luciferase assay or Western blotting. *P < 0.05 and **P < 0.01 vs. CON. B: PPRE activity in C2C12 myotubes cotransfected with pTK-PPREx3-luc and PPARδ vector was evaluated by luciferase assay. PPARδ expression in C2C12 myotubes transfected with pTK-PPREx3-luc was detected by Western blotting. Cells were treated with DMSO (CON) or indicated concentrations of TM (0.1–30 μmol/L) for 24 h. *P < 0.05 and **P < 0.01 vs. CON. C: Cells were treated with DMSO (CON) or 10 μmol/L TM for 24 h. Cells were treated with 10 μmol/L TM in the presence or absence of PPARδ inhibitor GSK0660 (GSK; 10 μmol/L), PPARγ inhibitor GW9662 (GW9662; 10 μmol/L), or PPARα inhibitor GW6471 (GW6471; 10 μmol/L) for 24 h before the luciferase assay. **P < 0.01 vs. CON; #P < 0.05 and ##P < 0.01 vs. TM 10 μmol/L; ΔP < 0.05 vs. TM 10 μmol/L plus GSK 10 μmol/L. D: 10 μmol/L TM treatment for 24 h increased the luciferase activity both in an empty pAdTrack expression vector as the control and the cotransfection with the PPARδ expression vector in transfected C2C12 myotubes. *P < 0.05 and **P < 0.01 versus CON; #P < 0.05 vs. PPARδ vector plus TM 10 μmol/L. E: PPARδ, PPARγ, and PPARα expression in C2C12 myotubes was detected by Western blotting after treatment with DMSO (CON) or TM (10 μmol/L) for 24 h. *P < 0.05 vs. CON. Data are mean ± SEM from 3–6 experiments.

FIG. 1. — Effect of TM on PPARδ expression and activity in C2C12 myotubes. A: PPRE activity in C2C12 myotubes transfected with pTK-PPREx3-luc was evaluated by luciferase assay. PPARδ expression in C2C12 myotubes transfected with pTK-PPREx3-luc was detected by Western blotting. C2C12 myotubes with cotransfection the plasmid pAdTrack-CMV-PPAR-δ, containing the full-length coding region of rat PPARδ (PPARδ vector), were treated with DMSO (control [CON]) or TM (10 μmol/L) for 15 min to 24 h before the luciferase assay or Western blotting. *P < 0.05 and **P < 0.01 vs. CON. B: PPRE activity in C2C12 myotubes cotransfected with pTK-PPREx3-luc and PPARδ vector was evaluated by luciferase assay. PPARδ expression in C2C12 myotubes transfected with pTK-PPREx3-luc was detected by Western blotting. Cells were treated with DMSO (CON) or indicated concentrations of TM (0.1–30 μmol/L) for 24 h. *P < 0.05 and **P < 0.01 vs. CON. C: Cells were treated with DMSO (CON) or 10 μmol/L TM for 24 h. Cells were treated with 10 μmol/L TM in the presence or absence of PPARδ inhibitor GSK0660 (GSK; 10 μmol/L), PPARγ inhibitor GW9662 (GW9662; 10 μmol/L), or PPARα inhibitor GW6471 (GW6471; 10 μmol/L) for 24 h before the luciferase assay. **P < 0.01 vs. CON; #P < 0.05 and ##P < 0.01 vs. TM 10 μmol/L; ΔP < 0.05 vs. TM 10 μmol/L plus GSK 10 μmol/L. D: 10 μmol/L TM treatment for 24 h increased the luciferase activity both in an empty pAdTrack expression vector as the control and the cotransfection with the PPARδ expression vector in transfected C2C12 myotubes. *P < 0.05 and **P < 0.01 versus CON; #P < 0.05 vs. PPARδ vector plus TM 10 μmol/L. E: PPARδ, PPARγ, and PPARα expression in C2C12 myotubes was detected by Western blotting after treatment with DMSO (CON) or TM (10 μmol/L) for 24 h. *P < 0.05 vs. CON. Data are mean ± SEM from 3–6 experiments.