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IFN‐γ induces apoptosis in mouse embryonic stem cells, a putative mechanism of its embryotoxicity
Author(s) -
Zou GangMing,
ReznikoffEtievant MarieFrançoise,
Hirsch François,
Milliez Jacques
Publication year - 2000
Publication title -
development, growth and differentiation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.864
H-Index - 66
eISSN - 1440-169X
pISSN - 0012-1592
DOI - 10.1046/j.1440-169x.2000.00511.x
Subject(s) - apoptosis , biology , embryonic stem cell , programmed cell death , microbiology and biotechnology , annexin , flow cytometry , embryo , interferon , trypan blue , immunology , genetics , gene
It has been reported that interferon (IFN)‐γ should inhibit in vitro mouse embryo growth by direct cell toxicity. However, the mechanism involved has not been clearly established. In the present study, this question was addressed using the embryonic stem (ES) cell model. It was found that IFN‐γ induces a dose‐dependent apoptosis in ES cells, as assessed by trypan‐blue staining, by Annexin‐V labeling and DNA analysis. Moreover, IFN‐γ treatment cooperates with Fas‐mediated apoptosis, a phenomenon that has been recently reported. As Bcl‐2 oncoprotein functions as a death repressor molecule in an evolutionarily conserved cell death pathway, its expression was analyzed by flow cytometry. It was demonstrated that Bcl‐2 is expressed in ES cells. When compared to untreated ES cells, IFN‐γ‐treated, apoptotic cells expressed a lower Bcl‐2 level and a normal level of Fas, whereas surviving cells expressed a normal level of Bcl‐2 but a lower Fas expression. Altogether, these data suggest that IFN‐γ may influence early mouse embryo development by promoting apoptosis, which may constitute a novel mechanism of IFN‐γ embryotoxicity.