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Updated: May 28, 2025

Intrauterine Telemetry to Measure Mouse Contractile Pressure In Vivo
Published on: April 6, 2015
Can activator protein-1 transcription factors be monitored in the maternal circulation to predict set on labor?
Toghrul Yahyayev1, Tugce Senturk Kirmizitas2, Ali Benian1
1Department of Obstetrics and Gynecology, Istanbul University - Cerrahpaşa, Cerrahpaşa Faculty of Medicine, Istanbul, Türkiye.
Objective:
We aimed to compare gene expression levels in myometrial tissues and serum from pregnant women undergoing cesarean section (CS) with and without uterine contractions. The myometrial activator protein-1 (AP-1) transcription factor family (JUN, FOS, and fos-related antigen-2 [FOSL2]) was evaluated as a contraction-related marker in maternal circulation to predict labor timing.
Methods:
Samples were collected from pregnant women undergoing CS. Uterine contractions were observed in the experimental group (n=10) but not in the control group (n=10). Gene expression of JUN, FOS, and FOSL2 was analyzed in serum and myometrial samples using droplet digital polymerase chain reaction, and statistical analysis was performed using GraphPad software (GraphPad Software, San Diego, CA, USA).
Results:
Given the non-normal data distribution, JUN, FOS, and FOSL2 gene expression levels increased in the CS group with uterine contractions. However, this increase was not statistically significant in either tissue or serum samples. Nevertheless, the correlation of JUN messenger RNA expression between maternal circulation and myometrial tissue was statistically significant in the CS group with contractions (p<0.01).
Conclusion:
This is the first study to investigate AP-1 transcription factor expression in matched tissue and serum samples in relation to uterine contractility. The increased expression of JUN, FOS, and FOSL2 in the CS group with contractions suggests these genes may play a key role in initiating or propagating human labor, indicating that contractionassociated AP-1 could serve as a biomarker for labor timing.
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