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Updated: Jul 27, 2025
Multiplexed Fluorescent Immunohistochemical Staining of Four Endometrial Immune Cell Types in Recurrent Miscarriage
Published on: August 4, 2021
MITA Promotes Macrophage Proinflammatory Polarization and Its circRNA-Related Regulatory Mechanism in Recurrent
Bowen Liu1, Jun Liu2, Yang Qiu3
1Hubei Clinic Research Center for Assisted Reproductive Technology and Embryonic Development, Reproductive Medical Center, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Abstract:
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.
Insights
MITA (STING) promotes miscarriage by increasing macrophage inflammation and apoptosis. A novel circRNA, circKIAA0391, exacerbates this by regulating the miR-512-5p/MITA pathway in decidual macrophages.
Area of Science:
- Immunology
- Molecular Biology
- Reproductive Medicine
Background:
- MITA (STING) is a key regulator of innate immunity and a potential therapeutic target.
- circRNA-mediated networks are crucial in gene regulation and disease.
- The role of MITA and its circRNA mechanisms in recurrent miscarriage (RM) are unknown.
Purpose of the Study:
- Investigate MITA's role in RM pathogenesis.
- Elucidate circRNA regulatory mechanisms involving MITA in RM.
- Determine the impact of MITA and circKIAA0391 on decidual macrophages.
Main Methods:
- Validated elevated decidual M1/M2 macrophage ratio in RM patients.
- Assessed MITA expression in decidual macrophages from RM patients.
- Utilized THP-1-derived macrophage (TDM) cells to study MITA's effects.
- Performed circRNA sequencing and bioinformatic analysis.
- Investigated the circKIAA0391/miR-512-5p/MITA axis.
Main Results:
- Decidual M1/M2 ratio is upregulated in RM patients.
- MITA is highly expressed in decidual macrophages of RM patients.
- MITA promotes apoptosis and pro-inflammatory polarization of TDM cells.
- A novel circRNA, circKIAA0391, is overexpressed in RM decidual macrophages.
- circKIAA0391 promotes TDM cell apoptosis and pro-inflammatory polarization via the miR-512-5p/MITA axis.
Conclusions:
- MITA plays a significant role in RM pathogenesis by influencing macrophage behavior.
- circKIAA0391 exacerbates RM by modulating the miR-512-5p/MITA pathway.
- This study provides insights into MITA's immunomodulatory function in RM.
