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Articles in PresS, published online ahead of print December 21, 2001
Am J Physiol Regu Physiol, 10.1152/ajpregu.00507.2001
Submitted on August 17, 2001
Accepted on November 7, 2001
1 Physiologisches Institut, Universitat Regensburg, Regensburg, Germany
2 Milano and FIRC Institute for Molecular Oncology, European Institute for Oncology, Milano, Italy
* To whom correspondence should be addressed. E-mail: stefanie.dragon{at}vkl.uni-regensburg.de.
During avian embryonic development, terminal erythroid differentiation occurs in the circulation. Some of the key events, like the induction of erythroid 2,3-bisphosphoglycerate (2,3BPG), carbonic anhydrase (CAII) and pyrimidine 5'-nucleotidase (P5N) synthesis is oxygen-dependent (3, 11-14, 34) in an indirect way: Hypoxia stimulates the release of norepinephrine (NE)/adenosine into the circulation (11, 13). This leads via erythroid ß-adrenergic/adenosine A2 receptor activation to a cAMP signal inducing several proteins in a transcription-dependent manner (11, 12, 17). -To understand how the cAMP-dependent processes are initiated, we screened an erythroid cDNA library for cAMP-regulated genes: We detected three genes that were strongly up-regulated (>5fold) by cAMP in definitive and primitive RBC. They are homologous to the mammalian Tob, Ifr1 and Fos proteins. In addition, the genes are induced in the intact embryo during short-term hypoxia. Since the genes are regulators of proliferation and differentiation in other cell types, we suggest that cAMP might promote general differentiating processes in erythroid cells thereby allowing adaptive modulation of the latest steps of erythroid differentiation during developmental hypoxia.
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