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. Author manuscript; available in PMC: 2011 Feb 5.
Published in final edited form as: Mol Cell Endocrinol. 2009 Aug 25;315(1-2):239. doi: 10.1016/j.mce.2009.08.014

Fig. 2.

Fig. 2

Relaxin increases the overall response to PPARγ agonists. HEK-RXFP1 cells were treated for 24 hours with or without 1nM relaxin in the presence or absence of specific PPAR agonists, then subject to the PPRE luciferase assay. The agonists used were WY-14,643 (WY, 2µM) for PPARα; GW-0742 (GW, 10nM) for PPARδ; and rosiglitazone (Rosi, 1µM) or 15-deoxy-Δ12,14-PGJ2 (PGJ2, 1µM) for PPARγ. The data are expressed as the ACO-PPRE luciferase activity relative to that in untreated cells, mean ± S.E.M (N=5). *p<.05 compared to corresponding agonist in the absence of relaxin; #p<.05 compared to no treatment; †p<.05 compared to either relaxin or corresponding agonist alone.