Fig. 4
PGE2-EP2 signaling mediates proinflammatory cytokine production in hMG. (A) qRT-PCR cycle thresholds of prostanoid receptor genes in unstimulated hMG (n = 3). (B) IL6 gene expression in hMG stimulated with vehicle or PGE2 ± prostanoid receptor antagonist for 2 h (n = 3–4). (C) IL1B and (D) CXCL8 gene expression in hMG stimulated with vehicle or PGE2 ± prostanoid receptor antagonist for 6 h (n = 3–4). (E) IL-6 protein levels in culture media from hMG stimulated with vehicle or PGE2 ± prostanoid receptor antagonist for 6 h (n = 3–4). (F) IL-8 protein levels in culture media from hMG stimulated with vehicle or PGE2 ± prostanoid receptor antagonist for 10 h (n = 3–4). (G) cAMP production from hMG stimulated with vehicle or elevating PGE2 concentrations for 15 min (n = 6). (H) cAMP production from hMG stimulated with vehicle or 1 μM PGE2 ± EP2 or EP4 antagonists for 15 min (n = 6). (I) IL6, (J) CXCL8, and (K) IL1B gene expression in hMG stimulated with vehicle or 100 pg/mL IL-1β ± EP2 antagonist for 6 h (n = 4). (L) IL6, (M) CXCL8, and (N) IL1B gene expression in hMG stimulated with vehicle or 250 μM palmitic acid ± EP2 antagonist for 24 h (n = 4). Data represent mean ± SD. One-way ANOVAs with Dunnett post-hoc tests were used for 4B-G. One-way ANOVAs with Tukey post-hoc tests were used for 4H-N. Statistically significant differences are represented as *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, ns (not significant) P > 0.05