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Differential effect of dexamethasone on cell death and STAT5 activation during in vitro eosinopoiesis
Author(s) -
DebierreGrockiego Françoise,
Fuentes Vincent,
Prin Lionel,
Gouilleux Fabrice,
GouilleuxGruart Valérie
Publication year - 2003
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1046/j.1365-2141.2003.04700.x
Subject(s) - glucocorticoid receptor , biology , haematopoiesis , stat protein , cellular differentiation , stat5 , microbiology and biotechnology , glucocorticoid , dexamethasone , eosinophil , apoptosis , stat3 , endocrinology , medicine , cancer research , immunology , signal transduction , stem cell , biochemistry , asthma , gene
Summary. Glucorticoids reduce eosinophilia through a direct effect on eosinophils or indirectly on cells producing cytokines and chemokines. Conflicting data have been previously reported concerning glucocorticoid effects on eosinopoiesis. To elucidate this point, dexamethasone was added during eosinophil differentiation of CD34 + cells. Dexamethasone enhanced proliferation and differentiation through an early effect on immature cells. Dexamethasone inhibited apoptosis during early differentiation, whereas death of mature cells was increased. Signal transducer and activator of transcription 5 (STAT5) is a transcription factor involved in the proliferation, differentiation and survival of haematopoietic cells, which interacts with glucocorticoid receptor. Activation of STAT5 by interleukin‐5 was investigated during eosinophil differentiation. Long isoforms of STAT5 were activated during the entire period in the culture as well as in blood eosinophils, while short isoforms were only activated during early differentiation. Short isoforms were less activated in the presence of dexamethasone. This suggests that dexamethasone could act on proliferation, differentiation and apoptosis during eosinophil differentiation through an association of STAT5 with the glucocorticoid receptor.