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Dörmer, P.* ; Spitzer, E. ; Möller, W.

EDR is a stress-related survival factor from stroma and other tissues acting on early haematopoitic progenitors (E-Mix).

Cytokine 27, 47-57 (2004)
DOI
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
The erythroid differentiation regulator (EDR) is a highly conserved autocrine factor produced in many tissues. Its haemoglobin synthesis-inducing activity for human and murine erythroleukaemia cell lines had been detected in WEHI-3 conditioned medium. EDR functions were analysed in detail. It is released from cells immediately in response to various stressful conditions and enhances cell survival particularly at a lower concentration range and low cell density. At high cell density and high EDR concentration the opposite effect of an increase in cell death was observed. Its essential function within a tissue is considered to be the maintenance of growth homeostasis. Cells kept in culture for weeks show a decreasing responsiveness to EDR supply. This was also noted in freshly cloned EDR-responsive mouse erythroleukaemia cells pointing to a molecular adaptation process. Human haematopoietic progenitors were amplified 7-fold by EDR when kept at low cytokine levels. At saturating levels progenitors giving rise to at least two lineages in semisolid medium (E-mix) respond to EDR with an average 1.87-fold increase in colony numbers and a bell-shaped dose–response curve. Of the more mature BFU-E compartment a response was observed particularly in cases with low colony numbers. Given the release from irradiated stromal cells and the ability to partly substitute for stromal cells in the Burkitt's lymphoma cell line BL-70, EDR functions as a stromal survival factor for stroma-responsive cells.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter survival factor; stress; stroma; BFU-E; E-mix
ISSN (print) / ISBN 1043-4666
e-ISSN 1096-0023
Zeitschrift Cytokine
Quellenangaben Band: 27, Heft: 2-3, Seiten: 47-57 Artikelnummer: , Supplement: ,
Verlag Elsevier
Verlagsort Oxford [u.a.]
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) CCG Inflammatory Lung Diseases (CPC-KEL)