PROBLEM Dendritic cells are the primary antigen-presenting cells that contact trophoblasts at the beginning of pregnancy. Excessive DCs maturity is described in some pregnancy complications, such as pre-eclampsia and fetal growth restriction, which are characterized by impaired trophoblast invasion. However, the mechanism is unclear. The long non-coding RNA long non-coding RNA DC (lnc-DC) is expressed exclusively in conventional human DCs and induces DC differentiation and maturation by promoting signal transducer and activator of transcription 3 (STAT3) phosphorylation. Our previous investigation proved lnc-DC and p-STAT3 are elevated in pre-eclampsia. This research is to study the mechanism of lnc-DC and trophoblast invasion. METHOD OF STUDY We transfected DCs with lnc-DC shRNA or a lentivirus for lnc-DC overexpression and cocultured these treated DCs with trophoblast under different conditions. Transwell assay and wound healing assay were used to detect the trophoblast invasion ability. We also tested the matured DCs and Th1 cells as well as the p-STAT3. RESULTS We found that lnc-DC promoted DC maturation and inhibited trophoblast invasion without the involvement of CD4+ T cells. And the p-STAT3 agonist could reverse the lnc-DC function. CONCLUSION Mature DCs may be involved in altering trophoblast invasion through the overexpression of lnc-DC, which increases p-STAT3 levels and the tissue inhibitor of metalloproteinase-1 (TIMP-1)/matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinase-2 (TIMP-2)/matrix metalloproteinase-2 (MMP-2) ratios. Thus, lnc-DC is a promising novel target for regulating trophoblast invasion.

中文翻译：

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树突状细胞中的长非编码RNA lnc-DC通过p-STAT3介导的TIMP / MMP表达调节滋养细胞的侵袭。

问题树突状细胞是在怀孕开始时与滋养细胞接触的主要抗原呈递细胞。DC的过度成熟被描述为某些妊娠并发症，例如先兆子痫和胎儿生长受限，其特征在于滋养层浸润受损。但是，机制尚不清楚。长非编码RNA长非编码RNA DC（lnc-DC）仅在常规人DC中表达，并通过促进信号转导子和转录激活因子3（STAT3）磷酸化来诱导DC分化和成熟。我们先前的研究证明子痫前期lnc-DC和p-STAT3升高。本研究旨在研究lnc-DC与滋养细胞侵袭的机制。研究方法我们用lnc-DC shRNA或慢病毒转染DC，以实现lnc-DC过表达，并在不同条件下将这些处理过的DC与滋养细胞共培养。用Transwell法和伤口愈合法检测滋养细胞侵袭能力。我们还测试了成熟的DC和Th1细胞以及p-STAT3。结果我们发现，lnc-DC可以促进DC成熟并抑制滋养细胞的侵袭，而无需CD4 + T细胞的参与。p-STAT3激动剂可以逆转lnc-DC功能。结论成熟的DC可能通过过量表达lnc-DC来改变滋养细胞的侵袭，从而增加p-STAT3水平以及金属蛋白酶-1（TIMP-1）/基质金属蛋白酶-9（MMP-9）的组织抑制剂和组织抑制剂金属蛋白酶2（TIMP-2）/基质金属蛋白酶2（MMP-2）的比率。从而，