ZFIN Image: Cha et al., 2005, Fig. 2

Image

Figure Caption

Fig. 2 PGE₂ and PGF_2α 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 PGF_2α 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.

Acknowledgments

This image is the copyrighted work of the attributed author or publisher, and ZFIN has permission only to display this image to its users. Additional permissions should be obtained from the applicable author or publisher of the image.

Reprinted from Developmental Biology, 282(1), Cha, Y.I., Kim, S.H., Solnica-Krezel, L., and Dubois, R.N., Cyclooxygenase-1 signaling is required for vascular tube formation during development, 274-283, Copyright (2005) with permission from Elsevier. Full text @ Dev. Biol.