Open AccessLIF/STAT3 Signaling Fails to Maintain Self‐Renewal of Human Embryonic Stem Cells
Author(s) -
Dahéron Laurence,
Opitz Sarah L.,
Zaehres Holm,
Lensch William M.,
Andrews Peter W.,
ItskovitzEldor Joseph,
Daley George Q.
Publication year - 2004
Publication title -
stem cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.159
H-Index - 229
eISSN - 1549-4918
pISSN - 1066-5099
DOI - 10.1634/stemcells.22-5-770
Subject(s) - leukemia inhibitory factor , embryonic stem cell , biology , leukemia inhibitory factor receptor , stat3 , microbiology and biotechnology , signal transduction , stem cell , glycoprotein 130 , stat protein , induced pluripotent stem cell , biochemistry , gene
Murine embryonic stem (mES) cells remain undifferentiated in the presence of leukemia inhibitory factor (LIF), and activation of signal transducer and activator of transcription 3 (STAT3) via LIF receptor (LIFR) signaling appears sufficient for maintenance of mES cell pluripotency. Anecdotal and contradictory accounts exist for the action of LIF in the culture of human embryonic stem cells, and the nature of LIF signaling and whether the LIF‐STAT3 pathway is conserved in human embryonic stem cells (hESCs) has not been systematically explored. In this study, we show that the LIFRβ and the signaling subunit gp130 are expressed in hESCs and that human LIF can induce STAT3 phosphorylation and nuclear translocation in hESCs. Nevertheless, despite the functional activation of the LIF‐STAT3 signaling pathway, human LIF is unable to maintain the pluripotent state of hESCs. Feeder‐free culture conditions that maintain hESCs in an undifferentiated state do not show activation of STAT3, suggesting that distinct signaling mechanisms govern the self‐renewal of hESCs.