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a Whitehead Institute for Biomedical Research, Cambridge, and Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Division of Pediatric Hematology/Oncology, The Children’s Hospital and Dana Farber Cancer Institute, Boston, Massachusetts, USA;
b Department of Biomedical Science, University of Sheffield, Western Bank, Sheffield, United Kingdom;
c Technion University, Rambam Medical Center, Haifa, Israel
Key Words. Human embryonic stem cells • Leukemia inhibitory factor • STAT3 • Self-renewal
Correspondence: George Q. Daley, M.D., Ph.D., Children’s Hospital, 300 Longwood Avenue, Boston, Massachusetts 02115, USA. Telephone: 617-919-2013; Fax: 617-730-0222; e-mail: george.daley{at}childrens.harvard.edu
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 LIFRß 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.
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