IL-36 cytokines (the agonists IL-36α, IL-36β, IL-36γ, and the antagonist IL-36Ra) are expressed in the mouse uterus and associated with maternal immune response during pregnancy. Here, we characterize the expression of IL-36 members in human primary trophoblast cells (PTC) and trophoblastic cell lines (HTR-8/SVneo and JEG-3) and upon treatment with bacterial and viral components. Effects of recombinant IL-36 on the migration capacity of trophoblastic cells, their ability to interact with endothelial cells and the induction of angiogenic factors and miRNAs (angiomiRNAs) were examined. Constitutive protein expression of IL-36 (α, β, and γ) and their receptor (IL-36R) was found in all cell types. In PTC, transcripts for all IL-36 subtypes were found, whereas in trophoblastic cell lines only for IL36G and IL36RN. A synthetic analog of double-stranded RNA (poly I:C) and lipopolysaccharide (LPS) induced the expression of IL-36 members in a cell-specific and time-dependent manner. In HTR-8/SVneo cells, IL-36 cytokines increased cell migration and their capacity to interact with endothelial cells. VEGFA and PGF mRNA and protein, as well as the angiomiRNAs miR-146a-3p and miR-141-5p were upregulated as IL-36 response in PTC and HTR-8/SVneo cells. In conclusion, IL-36 cytokines are modulated by microbial components and regulate trophoblast migration and interaction with endothelial cells. Therefore, a fundamental role of these cytokines in the placentation process and in response to infections may be expected.
Although there are plenty of evidence that dysregulation of microRNA (miRNA) level is involved in many human diseases, it is still unknown whether abnormal levels of specific miRNAs are associated with recurrent pregnancy loss (RPL). We believe that such an association do exist as this study confirmed significant differences in the level of specific miRNAs between RPL cases and healthy controls. The study was conducted on 100 Palestinian women: 60 patients with at least two unexplained consecutive pregnancy losses half of them were pregnant at the first trimester and the rest were non-pregnant and 40 healthy controls with at least two live births and no history of pregnancy loss; half of them were at their first trimester of pregnancy and the rest were non-pregnant. We investigated the relative expression of miR-21, miR-126, miR-155, miR-182, miR-222 and miR-517* using quantitative real-time polymerase chain reaction and Ct method experiments. Differential expression was evaluated using Student t-test and fold change analyses. The expression difference of miR-21, miR-126 and miR-182 between patients and controls in the pregnant subjects showed statistically significant difference (p-value ≤ 0.05) with fold decrease of 1.5, 1.6 and 5.6, respectively. In the non-pregnant group miR-21, miR-126, miR-222 and miR-517* expressions were significantly different with fold decrease of 2.4, 2.9, 2.7 and 11.8, respectively. In conclusion, at least miR-21 and miR-126 could serve as potential markers for idiopathic RPL as their levels were significantly lower in patients before being pregnant and during pregnancy. Moreover, restoration of the normal level of those miRNAs might be a novel intervention strategy in unexplained RPL. [Int J Reprod Contracept Obstet Gynecol 2013; 2(3.000): 330-335
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