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Preterm labor is a prevalent public health problem and occurs when the myometrium, the smooth muscle layer of the uterus, begins contracting before the fetus reaches full term. Abnormal contractions of the myometrium also underlie painful menstrual cramps, known as dysmenorrhea. Both disorders have been associated with increased production of prostaglandins and cytokines, yet the functional impacts of inflammatory mediators on the contractility of human myometrium have not been fully established, in part due to a lack of effective model systems. To address this, we engineered human myometrial microtissues (μmyometrium) on compliant hydrogels designed for traction force microscopy. We then measured μmyometrium contractility in response to a panel of compounds with known contractile effects and inflammatory mediators. We observed that prostaglandin F2α, interleukin 6, and interleukin 8 induced contraction, while prostaglandin E1 and prostaglandin E2 induced relaxation. Our data suggest that inflammation may be a key factor modulating uterine contractility in conditions including, but not limited to, preterm labor or dysmenorrhea. More broadly, our μmyometrium model can be used to systematically identify the functional impact of many small molecules on human myometrium.