BMC pregnancy and childbirth · 2025
The study of JAZF1-mediated apoptosis of decidual stromal cells by activating the NF-κB signaling pathway in spontaneous preterm birth.
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Gong Mei-Qin, Hu Ya-Yi, Zhang Yong-Qing, Wang Xiao-Dong
Аннотация
PURPOSE: Juxtaposed with another zinc finger gene 1 (JAZF1) is known to be involved in various biological processes, including gluconeogenesis, insulin sensitivity, cell differentiation, lipid metabolism, and inflammation. However, its role in spontaneous preterm birth (SPTB) remains unclear.
PATIENTS AND METHODS: We investigated the expression of JAZF1 mRNA using quantitative reverse transcription-PCR (qRT-PCR) in the decidual tissue of patients with SPTB compared to non-spontaneous preterm birth(non-SPTB). We also utilized Western blotting and ELISA to assess JAZF1 expression in peripheral blood from SPTB and non-SPTB patients. To further explore JAZF1's role, we validated the findings by constructing both knockdown and overexpression cellular models. The apoptosis level of decidual cells was detected by flow cytometry, and Western blotting was used to measure the expression of BCL-2, BAX, IκBα, phosphorylated IκBα, and COX-2. All collected data were statistically analyzed using GraphPad Prism 9.0. Gestational age was determined by crown-rump length (CRL) measured at 11-13+6 weeks. We compared the means between the two sample groups using either the independent sample t-test or the Wilcoxon rank-sum test, depending on the data distribution.
RESULTS: The JAZF1 expression in peripheral blood and decidual tissue of SPTB patients was significantly lower than that in non-SPTB patients. Moreover, the level of apoptosis in decidual stromal cells was notably higher in SPTB. JAZF1 knockdown significantly reduced decidual stromal cells' migration and invasion capabilities while promoting apoptosis, additionally, knocking down JAZF1 in decidual stromal cells elevated Bax expression and the phosphorylation of IκBα, decreasing BCL-2 expression, further promotes the release of factors associated with uterine contractions, while contrasting outcomes were observed in the overexpression experiment.
CONCLUSION: The identification of JAZF1 as a reliable molecular marker for spontaneous preterm labor offers novel insights for developing early warning biomarkers or targeted therapies.
PATIENTS AND METHODS: We investigated the expression of JAZF1 mRNA using quantitative reverse transcription-PCR (qRT-PCR) in the decidual tissue of patients with SPTB compared to non-spontaneous preterm birth(non-SPTB). We also utilized Western blotting and ELISA to assess JAZF1 expression in peripheral blood from SPTB and non-SPTB patients. To further explore JAZF1's role, we validated the findings by constructing both knockdown and overexpression cellular models. The apoptosis level of decidual cells was detected by flow cytometry, and Western blotting was used to measure the expression of BCL-2, BAX, IκBα, phosphorylated IκBα, and COX-2. All collected data were statistically analyzed using GraphPad Prism 9.0. Gestational age was determined by crown-rump length (CRL) measured at 11-13+6 weeks. We compared the means between the two sample groups using either the independent sample t-test or the Wilcoxon rank-sum test, depending on the data distribution.
RESULTS: The JAZF1 expression in peripheral blood and decidual tissue of SPTB patients was significantly lower than that in non-SPTB patients. Moreover, the level of apoptosis in decidual stromal cells was notably higher in SPTB. JAZF1 knockdown significantly reduced decidual stromal cells' migration and invasion capabilities while promoting apoptosis, additionally, knocking down JAZF1 in decidual stromal cells elevated Bax expression and the phosphorylation of IκBα, decreasing BCL-2 expression, further promotes the release of factors associated with uterine contractions, while contrasting outcomes were observed in the overexpression experiment.
CONCLUSION: The identification of JAZF1 as a reliable molecular marker for spontaneous preterm labor offers novel insights for developing early warning biomarkers or targeted therapies.