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A non‐apoptotic role for Fas/FasL in erythropoiesis
Author(s) -
Carlile Graeme W.,
Smith Deborah H.,
Wiedmann Martin
Publication year - 2009
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2009.01.047
Subject(s) - erythropoiesis , fas ligand , apoptosis , microbiology and biotechnology , fas receptor , caspase , biology , caspase 8 , programmed cell death , immunology , medicine , genetics , anemia
Issues remain to be elucidated in the developmental regulation of erythropoiesis. In particular the role of Fas, a member of the tumor necrosis factor family of receptors despite much work remains unclear. During erythropoiesis, Fas is expressed at low levels on erythroblasts. For most cell types, Fas to FasL interaction causes apoptotic cell death via caspase activation. Here, we show that in humans, early erythroid progenitors are refractory to apoptosis triggered through Fas. Further during early human erythropoiesis, Fas triggered caspase activation provides a positive stimulus for erythroid maturation, and does not alter cellular proliferation or trigger apoptosis.