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. Author manuscript; available in PMC: 2013 Feb 1.
Published in final edited form as: Mol Carcinog. 2011 Mar 22;51(2):139–149. doi: 10.1002/mc.20770

Figure 3. Cannabinoid receptors do not regulate AEA-induced cell death in JWF2 keratinocytes.

Figure 3

(A). AEA-induces cell death in a cannabinoid receptor-independent manner. Cells were pretreated with of 0.1, 0.5. 1.0, 5.0 or 10 µM SR141716 in the presence (20µM AEA) or absence (EtOH) of AEA. (B) Cells were pretreated with the CB2R antagonist, SR144528 at a final concentration of 0.2, 0.4, 2.0, 4.0, or 20 µM in the presence (20µM AEA) or absence (EtOH) of AEA. (C) Cells were pretreated with the TRPV1 channel inhibitor, capsazepine at a final concentration of 0.005, 0.05, 0.5, 5, and 50 µM in the presence (20µM AEA) or absence (EtOH) of AEA. As a negative control, cells remained untreated or were treated with the appropriate vehicle (ethanol or DMSO). Cells were incubated for 18 hours and viability measured in MTS experiments. The viability of cells treated with AEA plus the receptor antagonists was not statistically significantly different from cells treated with AEA alone. (D). Effect of AEA on cannabinoid receptor expression. JWF2 keratinocytes were treated with 20 µM AEA or ethanol and cells harvested at 1, 2, 4, and 6 hours. Cellular levels of CB1R, CB2R and TRPV1 were determined by conducting Western blot analysis.