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J Biol Chem, Vol. 274, Issue 25, 17813-17819, June 18, 1999

Mouse ATF-2 Null Mutants Display Features of a Severe Type of Meconium Aspiration Syndrome

Toshio MaekawaDagger §, François BernierDagger , Motohiko Sato, Shintaro Nomura§, Mandavi Singhparallel , Yoshiro Inoueparallel , Tomoyuki Tokunaga**, Hiroshi Imai**, Minesuke YokoyamaDagger Dagger , Andreas Reimold§§, Laurie H. Glimcher§§, and Shunsuke IshiiDagger §

From the Dagger  Laboratory of Molecular Genetics, Tsukuba Life Science Center, RIKEN, 3-1-1 Koyadai, Tsukuba, Ibaraki 305-0074, Japan, the  Department of Pathology, Osaka University Medical School, 2-2 Yamada-oka, Suita, Osaka 565-0871, Japan, the parallel  Department of Anatomy, Hokkaido University School of Medicine, Sapporo, Hokkaido 060-0815, Japan, the ** National Institute of Animal Industry, 2 Ikenodai, Kukisaki, Inashiki, Ibaraki 305-0901, Japan, the Dagger Dagger  Mitsubishi Kagaku Institute of Life Sciences, 11 Minami-Ohya, Machida, Tokyo 194-0031, Japan, the §§ Department of Cancer Biology, Harvard School of Public Health, and Department of Medicine, Harvard Medical School, Boston, Massachusetts 02115, and the § CREST (Core Research for Evolutional Science and Technology), JST (Japan Science and Technology Corporation)

Mouse null mutants of transcription factor ATF-2 were generated by the gene targeting method. They died shortly after birth and displayed symptoms of severe respiratory distress with lungs filled with meconium. These features are similar to those of a severe type of human meconium aspiration syndrome. The increased expression of the hypoxia inducible genes suggests that hypoxia occurs in the mutant embryos and that it may lead to strong gasping respiration with consequent aspiration of the amniotic fluid containing meconium. A reduced number of cytotrophoblast cells in the mutant placenta was found and may be responsible for an insufficient supply of oxygen prior to birth. Using the cDNA subtraction and microarray-based expression monitoring method, the expression level of the platelet-derived growth factor receptor alpha  gene, which plays an important role in the proliferation of trophoblasts, was found to be low in the cytotrophoblasts of the mutant placenta. In addition, ATF-2 can trans-activate the PDGF receptor alpha  gene promoter in the co-transfection assay. These results indicate the important role of ATF-2 in the formation of the placenta and the relationship between placental anomalies and neonatal respiratory distress. The ATF-2 null mutants should enhance our understanding of the mechanism of severe neonatal respiratory distress.

Copyright © 1999 by The American Society for Biochemistry and Molecular Biology, Inc.
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