The Herington laboratory is focused on interventional approaches to regulate uterine contractions and efforts to better understand the mechanism of uterine contractility. Current treatments are limited in scope and efficacy, often adversely affecting both the mother and her offspring. Our laboratory has established a drug discovery strategy to identifying novel regulators of uterine myometrial contractility. Our laboratory is equipped for high-throughput screening of small-molecules using an in vitro cell-based assay, testing of hit-molecules in an ex vivo tissue contractility assay and pre-clinical in vivo testing in mouse models of preterm labor. Other experimental approaches include: traditional cell/molecular biology to elucidate mechanisms of action. Our laboratory utilizes mouse and human uterine myometrial tissue samples, mouse models of preterm labor, and transgenic mouse models of delayed parturition.

My commitment to a career focused on maternal-fetal interactions during pregnancy and labor was initiated during my doctoral studies, where I established in vivo mouse models to examine the important effect of the embryo on maternal uterine changes necessary for the establishment of pregnancy. Specifically, use of mouse models of artificially-induced decidualization, allowed examination into the molecular and paracrine signaling between the embryo and uterus during the processes of implantation and decidualization. I have continued interests and enthusiasm in research centered on maternal-fetal interactions during early pregnancy. Through current collaborations with Dr. Bibhash C. Paria's, I have been fortunate to assist with research projects focused on: 1) improved understanding of the process of blastocyst implantation using mouse and hamster models and 2) exploring new therapeutic strategies for attenuating endotoxin-induced early pregnancy defects.

While a postdoctoral fellow under the mentorship of Dr. Jeff Reese, I evaluated the mechanisms responsible for the delayed parturition phenotype of cyclooxygenase-1 knockout (Cox-1KO) mice. While unhindered uterine contractile function was observed in Cox-1KO pregnant females, an impaired cervical dilation phenotype was determined to contribute to parturition phenotype of these mice. Dr. Reese and I continue collaborative efforts to examine uterine and cervical function in mouse models of delayed parturition. Specifically, we utilize in vivo Raman spectroscopy to assess in vivo assessment cervical molecular changes during normal and impaired cervical remodeling in mouse models used to study pregnancy.