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Opposing roles of inter-α-trypsin inhibitor heavy chain 4 in recurrent pregnancy loss

机译：α-胰蛋白酶抑制剂重链4在复发性流产中的相反作用

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Background The mechanism behind an increased risk of recurrent pregnancy loss (RPL) remains largely unknown. In our previous study, we identified that inter-α-trypsin inhibitor heavy chain 4 (ITI-H4) is highly expressed at a modified molecular weight of 36?kDa in serum derived from RPL patients. Yet, the precise molecular mechanism and pathways by which the short form of ITI-H4 carries out its function remain obscure. Methods Human sera and peripheral blood mononucleated cells (PBMCs) were collected from patients and normal controls to compare the expression levels of ITI-H4 and plasma kallikrein (KLKB1). Flow cytometric assay was performed to measure inflammatory markers in sera and culture supernatants. Furthermore, to investigate the functions of the two isoforms of ITI-H4, we performed migration, invasion, and proliferation assays. Findings In the current study, we showed that ITI-H4 as a biomarker of RPL could be regulated by KLKB1 through the IL-6 signaling cascade, indicating a novel regulatory system for inflammation in RPL. In addition, our study indicates that the two isoforms of ITI-H4 possess opposing functions on immune response, trophoblast invasion, and monocytes migration or proliferation. Interpretation The ITI-H4 (?Nsup688/sup) might be a crucial inflammatory factor which contributes to the pathogenesis of RPL. Moreover, it is expected that this study would give some insights into potential functional mechanisms underlying RPL. Fund This study was supported by the Ministry of Health & Welfare of the Republic of Korea (HI18C0378) through the Korea Health Industry Development Institute.
机译：背景反复流产（RPL）风险增加的背后机制尚不清楚。在我们之前的研究中，我们确定了间-α-胰蛋白酶抑制剂重链4（ITI-H4）在RPL患者血清中的修饰分子量为36？kDa时高表达。然而，ITI-H4的短形式发挥其功能的精确分子机制和途径仍然不清楚。方法收集患者和正常对照组的人血清和外周血单核细胞（PBMC），比较ITI-H4和血浆激肽释放酶（KLKB1）的表达水平。进行流式细胞术测定以测量血清和培养上清液中的炎性标志物。此外，为了研究ITI-H4两种同工型的功能，我们进行了迁移，侵袭和增殖分析。结果在当前研究中，我们表明ITI-H4作为RPL的生物标志物可以通过IL-6信号级联反应被KLKB1调控，这表明RPL中炎症的新型调控系统。此外，我们的研究表明，ITI-H4的两种同工型在免疫反应，滋养细胞入侵和单核细胞迁移或增殖方面具有相反的功能。解释ITI-H4（？N 688 ）可能是导致RPL发病的关键炎症因子。此外，预计该研究将对RPL的潜在功能机制提供一些见识。基金本研究由大韩民国卫生和福利部（HI18C0378）通过大韩民国卫生产业发展研究所提供支持。

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