To Die or Not to Die: the Function of the Transcription Factor NF-κB in Embryos Exposed to Stress


Address reprint requests to A. Torchinsky, Department of Cell and Developmental Biology, Sackler School of Medicine, Tel-Aviv University, Ramat Aviv, Tel Aviv, 69978, Israel.


Background:  Cytokines operating in the embryo and embryonic microenvironment determine, to a significant extent, whether pregnancy is completed successfully or results in embryonic loss or maldevelopment. They act as activators of specific transcription factors, which control cell responses such as cell proliferation differentiation and apoptosis. One such transcription factor is the nuclear factor-κB (NF-κB), which is presently seen as a key molecule controlling the apoptosis process. In the light of evidence that a majority of embryopathic stresses, regardless of their nature, first disturb the apoptotic process, it is conceivable, that NF-κB may play an important role in regulating the resistance of embryos to embryopathic stresses. In this brief review, we discuss such a possibility based on data characterizing expression and function of NF-κB in the embryo and extraembryonic tissues during normal embryogenesis as well as after exposure to various embryopathic stresses.

Methods:  Critical review of existing data.

Results:  Data summarized in this review suggest that (a) practically all NF-κB/Rel family members are expressed in embryonic, trophoblast and uterine cells in a developmental stage- and cell type-specific manner; (b) NF-κB-mediated anti-apoptotic signaling in embryonic cells seems to be indispensable for proper development during the organogenesis stage, (c) NF-κB activity in stress-targeted embryonic and extraembryonic structures directly correlates with their ability to resist stress-induced process of embryo loss and maldevelopment.

Conclusion:  Data presented in this review suggest that NF-κB may act as a protector of embryos exposed to embryopathic stresses, possibly, because of the ability of NF-κB to prevent the induction of programmed cell death as well as to activate cell proliferation.