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. Author manuscript; available in PMC: 2013 May 6.
Published in final edited form as: Prostaglandins Other Lipid Mediat. 2011 Jul 27;96(0):54–62. doi: 10.1016/j.prostaglandins.2011.07.005

Fig. 3.

Fig. 3

Effect of EET-agonist on the levels of PPARγ, FAS, Wnt/β-catenin and pACC. (A) hMSCs-derived adipocytes expressed elevated levels of PPARγ and FAS. Western blots showed that EET-agonist sustained decrease in PPARγ and FAS and simultaneous decrease in β-catenin and pACC. (B) Densitometric evaluations of protein were obtained from three different experiments. Data are expressed as mean ± SE (*p < 0.05 versus untreated 2 days MSCs-derived adipocyte growth). (C) adipogenic markers including PPARγ and SREBP-1 mRNA expression analyzed by quantitative PCR in 10 days culture treated and untreated with EET-agonist. Results for each condition are expressed as mean ± SE (n = 6, *p < 0.05 versus EET-agonist treated).

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