Fig. 5.

Involvement of PPARα and TRPV1 in the promigratory effect of URB597, AA-5HT, endocannabinoids, and endocannabinoid-like substances on MSCs. A–D: MSCs were pretreated with the PPARα antagonist, GW6471 (GW) (10 μM), for 1 h and subsequently incubated with vehicle or the FAAH inhibitors URB597 and AA-5HT (A) (10 μM each), the endocannabinoids AEA and 2-AG (B) (10 μM each), or the endocannabinoid-like substances OEA (C) and PEA (D) (10 μM each) for another 6 h. In the case of OEA (C) and PEA (D), cells were likewise pretreated with the TRPV1 antagonist, capsazepine (Capsa, 1 μM), for 1 h. E: Concentration-dependent increase of migration by PPARα activation. MSCs were incubated with the selective PPARα agonist, WY-14643, at the indicated concentrations for 6 h. In all experiments, migration was assessed by Boyden chamber assays. Percent control represents mean ± SEM in comparison to vehicle-treated cells (100%) of n = 4 (A–D) or n = 3–4 (E) experiments using cells obtained from one donor. *P < 0.05 versus vehicle; ^#P < 0.05 versus respective test substance in the absence of antagonists, one-way ANOVA plus post hoc Bonferroni (A–D) or Dunnett test (E).