Hemoglobin F synthesis in vitro: evidence for control at the level of primitive erythroid stem cells.

Papayannopoulou, T; Brice, M; Stamatoyannopoulos, George

doi:10.1073/pnas.74.7.2923

Cited by 199 publications

(58 citation statements)

References 16 publications

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“…The technique we used for BFUe cultures has been described in detail (6,7). Plates from the days of peak hemoglobin formation were used for labeling with monospecific anti-hemoglobin antibodies.…”

Section: Methodsmentioning

confidence: 99%

“…Studies of individual erythroid bursts with fluorescent anti-Hb antibodies have revealed striking differences in expression of Hb F among erythroid bursts (7). Most significantly, differences in the expression of Hb F can exist among the subclones in a burst originating from a single cell (7).…”

mentioning

confidence: 99%

“…F cells contain both Hb A and Hb F, and they are derived from the same pluripotent stem-cell progenitors as the erythrocytes that fail to express Hb F (3)(4)(5). When erythroid progenitors [erythroid burst-forming unit(s); BFUe(s)] from adult persons are used for culture, reactivation of Hb F synthesis appears in the clones (6)(7)(8)(9). Hence, cultures of BFUes provide a tool for investigating the cellular mechanisms controlling the expression of Hb F in adult cells.…”

mentioning

confidence: 99%

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Stochastic expression of fetal hemoglobin in adult erythroid cells.

Stamatoyannopoulos¹,

Kurnit²,

Papayannopoulou³

1981

Proc. Natl. Acad. Sci. U.S.A.

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The expression of fetal hemoglobin, Hb F, in the adult cells is cellularly restricted both in vivo and in culture. Because, in cultures of erythroid progenitors, subclones that express or fail to express Hb F are derived from the same erythroid stem cell, a mechanism must exist whereby Hb F expression segregates in the progeny of erythroid progenitors during their differentiation. We present mathematical analyses of experimental data which suggest that expression of Hb F in human adult erythroid cells occurs on a stochastic basis. We quantified Hb F expression among the subclones of erythroid bursts (clones) in vitro by labeling subclones with fluorescent anti-Hb F antibodies. The observed data were compared with predictions from a stochastic model with the assumption that the expression of Hb F in a subclone occurs with a probability P equal to the frequency of Hb F-expressing subclones in an experiment. There was good fit between the observed and predicted data with respect to: (i) the relative frequencies of monomorphic F+, monomorphic F-, and bimorphic F+/F- bursts, respectively; (ii) the size distributions among F+, F- and F+/F- bursts; and (iii) the proportions of subclones expressing Hb F within bimorphic F+/F- bursts. Given the hypothesis that erythroid progenitors which have an active Hb F program are less differentiated than cells which do not proceed to express Hb F, the stochastic event indicated by our analyses may be the probability that adult erythroid progenitor cells undergo terminal differentiation at an earlier stage than usual.

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Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Stochastic expression of fetal hemoglobin in adult erythroid cells.

Stamatoyannopoulos¹,

Kurnit²,

Papayannopoulou³

1981

Proc. Natl. Acad. Sci. U.S.A.

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“…K562 (22), HEL (24), Manca (27), Jurkat (41), and HL-60 (9) cells and Epstein-Barr virus (EBV)-transformed human lymphoblastoid cells (14) were propagated in suspension culture in RPMI 1640 with 2 mM L-glutamine, 10% fetal calf serum, and antibiotics in a humidified 5% CO2 atmosphere at 37°C. Cultures of peripheral blood erythroid burst-forming units (BFU-e) were prepared and harvested as described previously (29).…”

mentioning

confidence: 99%

Translocation of an erythroid-specific hypersensitive site in deletion-type hereditary persistence of fetal hemoglobin.

Elder¹,

Forrester²,

Thompson³

et al. 1990

Mol. Cell. Biol.

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Hereditary persistence of fetal hemoglobin (HPFH) can involve large deletions which eliminate the 3' end of the ,8-like globin gene cluster and more than 70 kilobases (kb) of flanking DNA. Blot hybridization revealed a DNase I-hypersensitive site extending from 1.1 to 1.4 kb downstream of the HPFH-1 3' deletion endpoint. The site was found in normal fetal and adult nucleated erythroid cells and in two erythroleukemia cell lines but not in nonerythroid cells and tissues. Simian virus 40 core enhancer-like sequences were found nonrandomly distributed within the boundaries of the site, which is contained in a fragment of known enhancer activity (E. A. Feingold and B. G. Forget, Blood, in press). A second hypersensitive site was found 0.5 kb upstream of the HPFH-1 3' deletion endpoint but was not erythroid specific. A third site, most prominent in fetal liver-derived erythroid cells, was found 1 kb upstream of the HPFH-2 deletion endpoint. As predicted by the locations of the deletion endpoints, the first two sites were translocated to within 12 kb of the A_Y gene in erythroid colonies derived from an HPFH-2 heterozygote and in hybrid mouse-human erythroid cells carrying the HPFH-2 deletion chromosome. Further analysis of this region showed that it was DNase I sensitive in erythroid and myeloid cells, indicating that it resides in an open chromatin domain. These observations suggest that alterations of chromatin structure flanking the fetal globin genes may contribute to abnormal gene regulation in deletion-type HPFH.

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“…Fötal hemoglobinin ergin hemoglobine dönüşümü ile ilgili birçok araştırmalar yapılmış, bu araştırma sonuçlarına göre bu dönü-şümün nedeni alyuvarı oluşturan hücrelerin sayısına, başkalaşımına ve globin yapan genlerin değişimine bağlanmıştır (6,22,29,44).…”

Section: Introductionunclassified

Saglikli Buzagilarda Hemoglobi̇n Ve Fötal Hemoglobi̇n Düzeyleri̇'

Bağcı¹

1993

Ankara Üniversitesi Veteriner Fakültesi Dergisi

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Hemoglobin F synthesis in vitro: evidence for control at the level of primitive erythroid stem cells.

Cited by 199 publications

References 16 publications

Stochastic expression of fetal hemoglobin in adult erythroid cells.

Stochastic expression of fetal hemoglobin in adult erythroid cells.

Translocation of an erythroid-specific hypersensitive site in deletion-type hereditary persistence of fetal hemoglobin.

Saglikli Buzagilarda Hemoglobi̇n Ve Fötal Hemoglobi̇n Düzeyleri̇'

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