Literature DB >> 6155136

Fetal Hb production during acute erythroid expansion. I. Observations in patients with transient erythroblastopenia and post-phlebotomy.

T Papayannopoulou, E Vichinsky, G Stamatoyannopoulos.   

Abstract

In order to study fetal haemoglobin production during acute erythroid expansion we did sequential measurements of Hb F-containing erythrocytes (F-cells) and of relevant haematological parameters in 10 subjects recovering from eyrthroid aplasia, iron deficiency anaemia or following phlebotomy. An increased production of F-cells was consistently observed during the acute marrow expansion, but there were significant differences in the maximum F-cell response among individuals. These differences could not be explained by differences in the degree of anaemia alone, nor could they be correlated with the level of peak reticulocytosis. Two patients who reached the highest F-cell numbers were probably carriers of heterocellular hereditary persistence of Hb F, suggesting that this gene may play a role in determining the magnitude of F-cell production in anaemic patients. It is speculated that the main reason for the consistently observed increase in F cell production during acute marrow expansion is the premature terminal differentiation of earlier erythroid precursos (burst forming units; BFUe). This proposition is in accord with observations in vitro which suggest that Hb F is expressed en eyrthroid clones derived from BFUne's. It is further proposed that differences in the degree of BFUe recruitment may underly the disparities in Hb F response among individuals subjected to similar anaemic stimuli.

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Year:  1980        PMID: 6155136     DOI: 10.1111/j.1365-2141.1980.tb08707.x

Source DB:  PubMed          Journal:  Br J Haematol        ISSN: 0007-1048            Impact factor:   6.998


  22 in total

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Review 2.  Control of globin gene expression during development and erythroid differentiation.

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Review 3.  Fetal hemoglobin in sickle cell anemia.

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4.  Old genes for new: a possible approach to the management of some genetic diseases?

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5.  Fetal hemoglobin synthesis in vivo: direct evidence for control at the level of erythroid progenitors.

Authors:  T Umemura; A Al-Khatti; T Papayannopoulou; G Stamatoyannopoulos
Journal:  Proc Natl Acad Sci U S A       Date:  1988-12       Impact factor: 11.205

6.  Heterocellular hereditary persistence of fetal hemoglobin (HPFH). Molecular mechanisms of abnormal gamma-gene expression in association with beta thalassemia and linkage relationship with the beta-globin gene cluster.

Authors:  A Giampaolo; F Mavilio; N M Sposi; A Carè; A Massa; L Cianetti; M Petrini; R Russo; M D Cappellini; M Marinucci
Journal:  Hum Genet       Date:  1984       Impact factor: 4.132

Review 7.  Developmental genetics of the human haemoglobins.

Authors:  W G Wood; D J Weatherall
Journal:  Biochem J       Date:  1983-10-01       Impact factor: 3.857

Review 8.  Advances in the understanding of haemoglobin switching.

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Journal:  Br J Haematol       Date:  2010-03-01       Impact factor: 6.998

9.  Control of the simian fetal hemoglobin switch at the progenitor cell level.

Authors:  B P Alter; B T Jackson; J M Lipton; G J Piasecki; P L Jackson; M Kudisch; D G Nathan
Journal:  J Clin Invest       Date:  1981-02       Impact factor: 14.808

10.  SCF induces gamma-globin gene expression by regulating downstream transcription factor COUP-TFII.

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