Dr. England's long-term research interest lies in the role of ion channels in smooth muscle as they pertain to women's health. The main objective of her laboratory is to determine the role of ion channels in modulation of uterine and vascular smooth muscle excitability and contractility. One focus of the laboratory is to determine how alternative splice variants of calcium-activated K+ channels in the myometrium modulate uterine excitability and contractility during gestation and parturition. They study this using a multidisciplinary approach with molecular, biochemical, electrophysiological, and immunohistochemical techniques. Dr. England is also interested in the trafficking of this channel and genetic factors that aid in regulating uterine excitability in both non-pregnant and pregnant states. They have recently begun studies on how this channel behaves in the vascular system in response to hormonal challenges. Research aimed at smooth muscle relaxation will have a wide range of benefits including alleviation of uterine dysfunction that results in premature labor and enhanced relaxation of vascular smooth muscle.
Current Projects · Assessment of the regulation of maxi-K channel splice variants during gestation and parturition · Determination of the role of sex hormones in regulating alternative splicing of the maxi-K channel in uterine smooth muscle · Protein-trafficking of ion channels during parturition · Regulation of potassium channel expression and function in response to sex steroids in both the myometrium and vasculature · Identification of mechanisms causing cardiovascular risk during hormone replacement therapy
Publications 1) Benkusky, N.A., D. J. Fergus, T. M. Zucchero, and S.K. England (2000) Regulation of the Ca2+-sensitive domains of the maxi-K channel in the mouse myometrium during gestation. J. Biol. Chem. 275 (36): 27712-27719.
2) Korovkina, V.P., D.J. Fergus, A.J. Holdiman, and S.K. England (2001) Cloning and characterization of a novel 132 bp exon of the maxi-K channel in human myometrium. Am. J. Physiol.281 (1): C361-C367.
3) Korovkina, V.P. and S.K. England (2002) Molecular diversity of vascular potassium channel isoforms. Clin. Exp. Pharm. Physiol. 29: 317-323.
5) Korovkina, V.P. and S.K England (2002) Detection and implications of potassium channel alterations. Vasc. Pharm. 38 (1): 3-12.
6) Benkusky, N.A., V.P. Korovkina, A.M. Brainard, and S.K. England (2002) Myometrial maxi-K channel ß1 subunit modulation during pregnancy and after 17ß-estradiol stimulation. FEBS Lett. 524(1-3): 97-102.
7) Fergus, D.J., J. R. Martens, and S.K. England (2003) Kv channel subunits that contribute to voltage-gated K+ channel current in renal vascular smooth muscle. Pflügers Arch 445: 697-704.
8) Albarwani, S., Nemetz, L.T., Madden, J.A., Tobin, A.A., England, S.K., Pratt, P.F. and N.J. Rusch (2003) Voltage-gated K+ channels in small rat cerebral arteries: molecular identify of functional channels. J. Physiol. 551: 751-763.
9) Chen, C., Lamping, K.G., Nuno, D.W., Barresi, R. Prouty, S.J., Lavoie, J.L., Cribbs, L.L, England, S.K., Sigmund, C.D., Weiss, R.M., Williamson, R.A., Hill, J.A., and K.P. Campbell (2003) Abnormal coronary functions in mice deficient in a1H t-type Ca2+ channels. Science, 302(5649); 1416-1418.
10) Korovkina, V.P., A.M. Brainard, P. Ismail, T.J. Schmidt and S.K. England (2004) Estrogen binding to maxi-K channels induces their down regulation via proteasomal degradation. J. Biol. Chem., 279 (2); 1217-1223.
