MITA Promotes Macrophage Proinflammatory Polarization and Its circRNA-Related Regulatory Mechanism in Recurrent Miscarriage.
MITA Promotes Macrophage Proinflammatory Polarization and Its circRNA-Related Regulatory Mechanism in Recurrent Miscarriage.
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DOI：
10.3390/ijms24119545
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发表时间：
2023-05-31
影响因子：
5.6
通讯作者：
中科院分区：
文献类型：
--
作者：
MITA（也称为 STING）是 DNA 介导的先天免疫激活的主要调节因子，是病毒感染和病毒相关疾病的潜在治疗靶点。 circRNA介导的ceRNA网络在基因调控中发挥重要作用，并可能导致许多人类疾病。然而，MITA与复发性流产（RM）之间的关系及其circRNA相关调控机制仍不清楚。在这项研究中，我们验证了 RM 患者的蜕膜 M1/M2 比率上调，表明蜕膜巨噬细胞在 RM 发病机制中的重要作用。我们发现 MITA 在 RM 患者的蜕膜巨噬细胞中高表达，并验证 MITA 可以促进 THP-1 衍生巨噬细胞 (TDM) 细胞的凋亡和巨噬细胞促炎极化。通过circRNA测序和生物信息学分析，我们筛选出一种在RM患者蜕膜巨噬细胞中过度表达的新型circRNA（circKIAA0391）。从机制上讲，我们发现 circKIAA0391 可以通过海绵 miR-512-5p/MITA 轴来促进 TDM 细胞的凋亡和促炎极化。该研究为进一步了解MITA对巨噬细胞的影响及其circRNA相关调节机制提供了理论基础，其可能在RM的病理生理学中具有至关重要的免疫调节功能。
MITA (also called STING), a master regulator of DNA-mediated innate immune activation, is a potential therapeutic target for viral infection and virus-related diseases. The circRNA-mediated ceRNA network plays important roles in gene regulation and may contribute to many human diseases. However, the relationship between MITA and recurrent miscarriage (RM) and its circRNA-related regulatory mechanisms remain unclear. In this study, we validated that the decidual M1/M2 ratio was upregulated in RM patients, suggesting the vital roles of decidual macrophages in the pathogenesis of RM. We found that MITA was highly expressed in decidual macrophages of RM patients and validated that MITA could promote apoptosis and macrophage proinflammatory polarization in THP-1-derived macrophage (TDM) cells. Using circRNA sequencing and bioinformatic analysis, we screened out a novel circRNA (circKIAA0391) that is overexpressed in decidual macrophages of RM patients. Mechanistically, we found that circKIAA0391 could promote the apoptosis and proinflammatory polarization of TDM cells by sponging the miR-512-5p/MITA axis. This study provides a theoretical basis for further understanding the impact of MITA on macrophages and its circRNA-related regulatory mechanisms, which may have a crucial immunomodulatory function in the pathophysiology of RM.
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