Interleukin 25 induced by human chorionic gonadotrophin promotes the proliferation of decidual stromal cells by activation of JNK and AKT signal pathways
Interleukin-25 expression was enhanced by trophoblast-derived hCG, could stimulate the proliferation of DSCs through activating JNK and AKT signals, which finally contributes to the establishment and maintenance of physiological pregnancy.
Ying Wang, B.S., Yuan Zhang, B.S., Ming-Qing Li, Ph.D., M.D., Deng-Xuan Fan, M.S., Xiao-Hui Wang, B.S., Da-Jin Li, M.D., Ph.D., Li-Ping Jin, M.D., Ph.D.
Volume 102, Issue 1, Pages 257–263
To clarify the role and mechanism of interleukin (IL)-25 in regulating the biological functions of decidual stromal cells (DSCs) in human early pregnancy.
Laboratory study of the effect of IL-25 induced by hCG on the proliferation of DSCs.
Women aged 23–47 years with normal pregnancy and abortion.
Main Outcome Measure(s):
Signal transduction from IL-25.
Here we show that DSCs coexpress IL-25/IL-17RB. Human chorionic gonadotropin promotes the expression of IL-25/IL-17RB. In contrast to anti-human IL-25 neutralizing antibody, recombinant human IL-25 (rhIL-25) significantly stimulates the proliferation of DSCs in dosage- and time-dependent manners. RhIL-25 promotes the phosphorylation of AKT, extracellular-signal-regulated kinases 1/2 (ERK1/2), c-Jun N-terminal kinases (JNK), and nuclear factor κB in DSCs. Interestingly, blocking JNK or AKT signal with inhibitors down-regulates the stimulatory effect on DSC proliferation induced by rhIL-25. In addition, the results of Western blot show that the expression of IL-25/IL-17RB in DSCs from normal pregnancy was higher than that from abortion.
Our results have revealed that hCG derived of trophoblasts up-regulates the expression of IL-25/IL-17RB in DSCs and that IL-25 further stimulates the proliferation of DSCs through activating JNK and AKT signals, which finally contributes to the establishment and maintenance of physiological pregnancy.
Read the full text at: http://www.fertstert.org/article/S0015-0282(14)00266-0/fulltext