Monitoring of inflammatory preterm responses via myometrial cell based multimodal electrophysiological and optical biosensing platform.

Preterm birth (PTB) remains a leading cause of neonatal morbidity and mortality, with inflammation-induced PTB posing a significant challenge due to its complex pathophysiology. To address this, we developed an in vitro platform utilizing hTERT-immortalized human myometrial (hTERT-HM) cells integrated with a multielectrode array (MEA) biosensing system and optical calcium imaging. Compared to primary uterine myometrial cells, hTERT-HM cells exhibit superior reproducibility, high scalability, and convenient manipulation, facilitating the consistent and large-scale investigations. This advanced system facilitates simultaneous real-time monitoring of electrophysiological activity and intracellular calcium transient, providing detailed insights into uterine cell behavior during inflammatory PTB. Our study revealed that oxytocin (OT) induces regular contractions in hTERT-HM cells, and the synergistic effect of OT and lipopolysaccharide (LPS) disrupts electrophysiological patterns and calcium signaling, closely mimicking the pathophysiology of inflammation-induced PTB. Meanwhile, magnesium sulfate is validated to effectively suppress OT-induced calcium release and mitigate LPS-triggered irregular electrophysiological signals. By integrating advanced biosensing technologies and advantages of hTERT-HM cells, this platform offers a reliable, reproducible model to investigate the mechanisms of inflammation-driven PTB and further develop targeted therapeutic interventions.