Signaling Molecules Involved in IFN-γ-Inducible Nitric Oxide Synthase Expression in the Mouse Trophoblast
Article first published online: 23 OCT 2007
American Journal of Reproductive Immunology
Volume 58, Issue 6, pages 537–546, December 2007
How to Cite
Leanza, E. C., Hoshida, M. S., Costa, A. F., Fernandes, C. M., De Fatima Pereira Teixeira, C. and Bevilacqua, E. (2007), Signaling Molecules Involved in IFN-γ-Inducible Nitric Oxide Synthase Expression in the Mouse Trophoblast. American Journal of Reproductive Immunology, 58: 537–546. doi: 10.1111/j.1600-0897.2007.00537.x
- Issue published online: 9 NOV 2007
- Article first published online: 23 OCT 2007
- Submitted May 29, 2007; accepted August 24, 2007.
- Ectoplacental cone;
- JAK-STAT pathway
Problem We have previously shown that trophoblast can generate nitric oxide (NO) and express inducible isoform of nitric oxide synthase (iNOS). Moreover, this production was changed by the presence of interferon-γ (IFN-γ) establishing a relationship between trophoblast inductive response and this proinflammatory cytokine.
Method of study As the intracellular signal transduction pathway used by IFN-γ in target cells is the Janus kinase (JAK)-signal transducer and transcription activator (STAT), here we analyzed in the mouse trophoblast the effect of IFN-γ and staurosporine on mRNA and protein expressions of IFN-γ signaling molecules correlating them with iNOS expression.
Results Interferon-γ induced iNOS expression and upregulated Jaks and Stat1, but not Stat2 transcriptions. The protein distribution matched the mRNA expression pattern. These effects were abrogated when IFN-γ receptor was blocked by staurosporine.
Conclusion Due to the biological effects of NO-iNOS generated on induction of apoptosis and inflammatory responses, interaction between iNOS expression and IFN-γ-mediated signaling is very important for understanding the physiology of trophoblast at the maternal–fetal interface. Our data indicate IFN-γ acts specifically on trophoblast, regulating the expression of signaling molecules and is fundamental for iNOS expression.