Reference : Stat5 Is an Ambivalent Regulator of Neutrophil Homeostasis
Scientific journals : Article
Life sciences : Veterinary medicine & animal health
http://hdl.handle.net/2268/7934
Stat5 Is an Ambivalent Regulator of Neutrophil Homeostasis
English
Fievez, Laurence mailto [Université de Liège - ULg > Département de sciences fonctionnelles > Biochimie et biologie moléculaire >]
Desmet, Christophe [Université de Liège - ULg > > Biochimie et biologie moléculaire >]
Henry, Emmanuelle [Université Libre de Bruxelles - ULB > Laboratory of Animal Physiology, Institute of Molecular Biology and Medicine >]
Pajak, Bernard [Université Libre de Bruxelles - ULB > Laboratory of Animal Physiology, Institute of Molecular Biology and Medicine >]
Hegenbarth, Silke [University of Bonn (Germany) > Institute for Molecular Medicine and Experimental Immunology >]
Garze, Virginie [Université Libre de Bruxelles - ULB > Laboratory of Animal Physiology, Institute of Molecular Biology and Medicine >]
Bex, Françoise [Université Libre de Bruxelles - ULB > Laboratory of Microbiology, Institute for Microbiological Research J-M Wiame >]
Jaspar, Fabrice [Université de Liège - ULg > > Clinique des grands animaux >]
Boutet, Philippe [> > > >]
Gillet, Laurent [Université de Liège - ULg > > Immunologie et vaccinologie >]
Vanderplasschen, Alain [Université de Liège - ULg > > Immunologie et vaccinologie >]
Knolle, Percy A. [> > > >]
Leo, Oberdan [> > > >]
Moser, Muriel [> > > >]
Lekeux, Pierre mailto [Université de Liège - ULg > Département de sciences fonctionnelles > Physiologie >]
Bureau, Fabrice mailto [Université de Liège - ULg > Département de sciences fonctionnelles > Biochimie et biologie moléculaire >]
2007
PLoS ONE
Public Library of Science
2
1
e727
Yes (verified by ORBi)
International
1932-6203
San Franscisco
CA
[en] Although STAT5 promotes survival of hematopoietic progenitors, STAT5-/- mice develop mild neutrophilia. METHODOLOGY/PRINCIPAL FINDINGS: Here, we show that in STAT5-/- mice, liver endothelial cells (LECs) autonomously secrete high amounts of G-CSF, allowing myeloid progenitors to overcompensate for their intrinsic survival defect. However, when injected with pro-inflammatory cytokines, mutant mice cannot further increase neutrophil production, display a severe deficiency in peripheral neutrophil survival, and are therefore unable to maintain neutrophil homeostasis. In wild-type mice, inflammatory stimulation induces rapid STAT5 degradation in LECs, G-CSF production by LECs and other cell types, and then sustained mobilization and expansion of long-lived neutrophils. CONCLUSION: We conclude that STAT5 is an ambivalent factor. In cells of the granulocytic lineage, it exerts an antiapoptotic function that is required for maintenance of neutrophil homeostasis, especially during the inflammatory response. In LECs, STAT5 negatively regulates granulopoiesis by directly or indirectly repressing G-CSF expression. Removal of this STAT5-imposed brake contributes to induction of emergency granulopoiesis.
Researchers ; Professionals ; Students
http://hdl.handle.net/2268/7934

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