The Regulatory Role of Decidual RHOQ Downregulation on Aberrant Dendritic Cell Activation in Miscarriage

<title>Abstract</title> <p>Purpose Recurrent miscarriage (RSA) has an unexplained etiology in 52.4% of cases. Accurate prediction contributes significantly to improving pregnancy success rates while reducing gestational complications. This study identifies RHOQ as a predictor of abnormal immune status in miscarriage. Methods Key hub genes related to defective endometrial receptivity (DER) were identified through bioinformatic analysis. CIBERSORTx was used to assess immune infiltration status in DER patients and controls. Additionally, enrichment analyses were conducted to explore the pathways involved in DER. The immunoreactive score (IRS) was used to verify RHOQ expression and dendritic cell numbers in clinical samples. ELISA was used to measure the expression of inflammatory factors across different groups. Western blotting was used to measure CD40 and CD83 protein levels. Results The proportion of mature dendritic cells was significantly increased in patients with DER. RHOQ levels in decidual tissue from the DER group were markedly lower than those in the normal control (NC) group and negatively correlated with the number of mature dendritic cells. Clinical samples confirmed that the number of mature dendritic cells was greater in the RSA group than in the NC group. RHOQ expression was lower in decidual tissue from the RSA group and negatively correlated with the number of mature dendritic cells. The downregulation of RHOQ in human endometrial cells leads to DC maturation. Tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6) were upregulated in an RHOQ-silenced human endometrial epithelial cell line. Conclusion RHOQ can serve as a reliable biomarker for detecting abnormal immune status during pregnancy. Clinical trial registration This experiment is not a clinical trial.</p>