Heather Burkin: Regulation of uterine contraction and early labor prevention
Regulation of uterine contraction and early labor prevention
Research in my laboratory is focused on understanding the molecular mechanisms that promote uterine contraction and the onset of labor. Preterm birth is the leading cause of neonatal morbidity and mortality in the developed world and the long-term goal is to develop new therapies to promote uterine quiescence and allow a greater proportion of infants to be carried to term. Identification of new pharmacological agents to reduce uterine contraction would reduce preterm birth rates, reduce perinatal health disparities, and improve pregnancy outcomes, all of which have been identified as high priority research problems by the National Institutes of Health. My research has primarily focused on three related projects
The long-term goal of our research is to understand the regulation of uterine contraction and labor, and to develop new therapies to prevent infants form being born too early. Our laboratory was the first to show that metallopeptidase enzymes (MMP2 and MMP9) are elevated in the preterm laboring uterus, and that inhibition of these enzymes reduces contraction in human uterine tissue and delays birth in mice. We are currently working to determine if MMP inhibition prevents preterm birth in mouse models. Other projects in the lab include examining the effects of mechanical stretch, infection, and cannabinoids on uterine function. Finally, we have developed a 3D-bioprinted model of human uterine smooth muscle that we are working to characterize and improve for use in gene editing and drug discovery experiments. Techniques undergraduate students learn in our lab include cell culture, bioprinting, immunofluorescence and microscopy, nucleic acid and protein purification, qPCR, western blotting, working with mice, contraction experiments, and more!