Erythroid carbonic anhydrase and hsp70 expression in chick embryonic development: role of cAMP and hypoxia.
In the second half of avian embryonic development cAMP affects major aspects of red blood cell (RBC) function. At day 13/14, progressive developmental hypoxia causes the release of norepinephrine and erythroid beta-adrenergic receptor stimulation initiates the coordinate induction of adaptive key events of erythroid differentiation like carbonic anhydrase (CAII) and 2,3-biphosphoglycerate synthesis. Although cAMP-dependent regulation of CAII protein synthesis has been described in detail, no data exist about the transcriptional regulation in embryonic RBC. Here we report that after day 12 of embryonic development, the caII mRNA is accumulating. Hypoxic incubation at day 10 as well as in vitro incubation of isolated RBC with cAMP-elevating agonists strongly induces erythroid caII expression. The induction of caII occurs fast and does not require new protein synthesis. By screening several late erythroid genes, we could identify hsp70 as another cAMP-induced gene in definitive RBC. Because caII (but not hsp70) is also induced by cAMP in primitive RBC, the signal may regulate key events of late primitive and definitive erythropoiesis.[1]References
- Erythroid carbonic anhydrase and hsp70 expression in chick embryonic development: role of cAMP and hypoxia. Dragon, S., Baumann, R. Am. J. Physiol. Regul. Integr. Comp. Physiol. (2001) [Pubmed]
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