Sarah K. England

Sarah K. England is a physiologist and biophysicist and the Alan A. and Edith L. Wolff Professor of Obstetrics and Gynaecology at Washington University School of Medicine. England conducts research on cation channels in uterine smooth muscle to understand the biological correlates of preterm birth and is the Associate Program Director of the Prematurity Research Center at Washington University as well as the Vice Chair of Research for the Center for Reproductive Health Sciences. In 2005, England was selected as a Robert Wood Johnson Foundation Health Policy Fellow in the Office of Senator Hillary Clinton where she used her scientific expertise in obstetrics and gynaecology to guide policy changes.

Early life and education England was born in St. Paul, Minnesota. Her family moved to the Highland Park neighbourhood in 1969 after the Fair Housing Act was passed so that England and her four brothers could obtain a better quality education. She majored in biology and conducted research under the mentorship of John W. Osborn at the University of Minnesota in St. Paul studying the sympathetic nervous system response after barodenervation. This led to her first publication in the American Journal of Physiology in 1990. The potassium channels had a higher probability of open-state leading to increased potassium permeability and overall dysregulation of membrane excitability and contraction.

Following her graduate work, England pursued her postdoctoral work at Vanderbilt University under the mentorship of Michael M. Tamkun in the Department of Molecular Physiology and Biophysics. Her findings highlighted the possibility that potassium current diversity in the heart is in part due to the function and expression of beta subunits for voltage-gated potassium channels.

Career and research In 1997, England was appointed to the faculty at the University of Iowa, becoming an assistant professor in the Carver College of Medicine in the Departments of Molecular Physiology and Biophysics. She was also appointed special assistant to the Vice President of Medical Affairs at U of I.

England lead many educational programs to enhance diversity and inclusion in the institute. England became a co-director of the Iowa Biosciences Advantage Program, which is a National Institutes of Health funded program that aims to increase the participation and recruitment of minority students in biomedical graduate degrees. In addition to being a student mentor in the program, England worked hard to improve the program and make it an established and mainstay program at U of I. During this time, she helped draft legislations on issues related to her research on preterm birth and pregnancy, efficiently linking her science to policy changes. Funded by the March of the Dimes, England serves as Associate Program Director and Theme 3 Leader of the Prematurity Research Center at Washington University, working with a team of researchers across the university

England is also the Principal Investigator of the England Lab where she explores the physiology of ion channels in smooth muscle as a means to target these mechanisms in muscle diseases. She focuses on both vascular and uterine smooth muscle, with a specific focus on the implications of uterine ion channels in preterm birth.

Oxytocin and labor Another facet of England's research program focuses on the role of oxytocin in uterine contractility and how variations in response to oxytocin might lead to labor dysfunction. Oxytocin is a frequently used drug is obstetrics and gynaecology, and England was interested in exploring the safety of this frequent practice by characterizing women who require high doses of oxytocin for adequate cervical dilation during labor. They found that factors associated with higher necessary oxytocin dose were correlated with poor labor progress. The variants of oxytocin receptor that were predicted to interfere with oxytocin binding were enriched in women that required higher doses of oxytocin during pregnancy.

Chronodisruption and preterm birth England has also began an investigation of the role of chronobiology on preterm birth, through the Prematurity Research Center at WUSTL. The goal of this program is explore how disruptions to circadian rhythm affect the risk of preterm birth. They found that the time of onset and the amount of activity changes throughout pregnancy in both mice and women.

Awards and honors 2023 Elected to the National Academy of Medicine 2021 Distinguished Faculty Award, Founder's Day Washington University in St. Louis 2015 Alan A. and Edith L. Wolff Professor of Medicine Washington University in St. Louis 1996 UNCF-Merck Science Initiative Postdoctoral Science Research Fellowship

Select publications Amazu C, Ma X, Henkes C, Ferreira JJ, Santi CM, England SK. Progesterone and estrogen regulate NALCN expression in human myometrial smooth muscle cells. Am J Physiol Endocrinol Metab. 2020;318(4):E441-E452. doi:10.1152/ajpendo.00320.2019 McCarthy R, Jungheim ES, Fay JC, Bates K, Herzog ED, England SK. Riding the Rhythm of Melatonin Through Pregnancy to Deliver on Time. Front Endocrinol (Lausanne). 2019;10:616. Published 2019 Sep 13. doi:10.3389/fendo.2019.00616 Martin-Fairey CA, Zhao P, Wan L, et al. Pregnancy Induces an Earlier Chronotype in Both Mice and Women. J Biol Rhythms. 2019;34(3):323-331. doi:10.1177/0748730419844650 Reschke L, McCarthy R, Herzog ED, Fay JC, Jungheim ES, England SK. Chronodisruption: An untimely cause of preterm birth?. Best Pract Res Clin Obstet Gynaecol. 2018;52:60-67. doi:10.1016/j.bpobgyn.2018.08.001 Reinl EL, Goodwin ZA, Raghuraman N, et al. Novel oxytocin receptor variants in laboring women requiring high doses of oxytocin. Am J Obstet Gynecol. 2017;217(2):214.e1-214.e8. doi:10.1016/j.ajog.2017.04.036 Rada CC, Murray G, England SK. The SK3 channel promotes placental vascularization by enhancing secretion of angiogenic factors. Am J Physiol Endocrinol Metab. 2014;307(10):E935-E943. doi:10.1152/ajpendo.00319.2014 Li Y, Lorca RA, Ma X, Rhodes A, England SK. BK channels regulate myometrial contraction by modulating nuclear translocation of NF-κB. Endocrinology. 2014;155(8):3112-3122. doi:10.1210/en.2014-1152 Odibo AO, Rada CC, Cahill AG, et al. First-trimester serum soluble fms-like tyrosine kinase-1, free vascular endothelial growth factor, placental growth factor and uterine artery Doppler in preeclampsia. J Perinatol. 2013;33(9):670-674. doi:10.1038/jp.2013.33 England SK. From laboratory to legislation. Physiologist. 2007;50(3):91. Brainard AM, Korovkina VP, England SK. Disruption of the maxi-K-caveolin-1 interaction alters current expression in human myometrial cells. Reprod Biol Endocrinol. 2009;7:131. Published 2009 Nov 23. doi:10.1186/1477-7827-7-131 Holdiman AJ, Fergus DJ, England SK. 17beta-Estradiol upregulates distinct maxi-K channel transcripts in mouse uterus. Mol Cell Endocrinol. 2002;192(1-2):1-6. doi:10.1016/s0303-7207(02)00136-3 Benkusky NA, Fergus DJ, Zucchero TM, England SK. Regulation of the Ca2+-sensitive domains of the maxi-K channel in the mouse myometrium during gestation. J Biol Chem. 2000;275(36):27712-27719. doi:10.1074/jbc.M000974200 England SK, Uebele VN, Kodali J, Bennett PB, Tamkun MM. A novel K+ channel beta-subunit (hKv beta 1.3) is produced via alternative mRNA splicing. J Biol Chem. 1995;270(48):28531-28534. doi:10.1074/jbc.270.48.28531 England SK, Uebele VN, Shear H, Kodali J, Bennett PB, Tamkun MM. Characterization of a voltage-gated K+ channel beta subunit expressed in human heart. Proc Natl Acad Sci U S A. 1995;92(14):6309-6313. doi:10.1073/pnas.92.14.6309 England SK, Wooldridge TA, Stekiel WJ, Rusch NJ. Enhanced single-channel K+ current in arterial membranes from genetically hypertensive rats. Am J Physiol. 1993;264(5 Pt 2):H1337-H1345. doi:10.1152/ajpheart.1993.264.5.H1337 Osborn JW, England SK. Normalization of arterial pressure after barodenervation: role of pressure natriuresis. Am J Physiol. 1990;259(6 Pt 2):R1172-R1180. doi:10.1152/ajpregu.1990.259.6.R1172