PGE2 and PGF2α can rescue both gastrulation arrest and posterior mesoderm defects induced by indomethacin. Indomethacin treatment results in gastrulation arrest at 50 μM (A) and posterior mesoderm defects at 40 μM (B, arrow). Supplementing indomethacin with PGE2 or PGF2α can suppress both the gastrulation arrest (C, E) and posterior mesoderm defects (D). COX-2 inhibitors, NS-398, or celecoxib do not cause any noticeable phenotypic defects up to 150 μM (G). Two independent experiments were performed (n > 80) in indomethacin, celecoxib, and NS-398 treatment groups. In rescue experiments, we performed three independent experiments (n > 80) in each of the treatment groups.
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