Leslie Myatt PhD



Dr Leslie Myatt is Professor of Obstetrics and Gynecology and Co-Director of the Center for Pregnancy and Newborn Research at the University of Texas Health Science Center San Antonio. He moved to Texas in Jan 2009 having been a faculty member at the University of Cincinnati for 22 years and Director of the NIH-funded Physician Scientist Training Program (MD/PhD) and the Women’s Reproductive Health Research Scholars Program. Dr Myatt served as North American Editor of the journal Placenta (1997 to 2004), President of the Perinatal Research Society (1997), President of the International Federation of Placenta Associations (2002 to 2004) and President of the Society for Gynecologic Investigation (2009 to 2010).  Dr Myatt’s research interests are control of fetal placental vascular reactivity, the role of oxidative and nitrative stress in placental function and fetal programming and the regulation of prostaglandin synthesis and action in intrauterine tissues at parturition.  He has published over 200 papers and 300 abstracts and has served on many review panels and study sections for NIH, CIHR and other international grant giving bodies.



As the interface between mother and fetus the placenta fulfills nutrient transport and hormonal signaling functions to support optimal fetal growth and development. Alterations in these functions are found in several placental pathologies that ultimately lead to adverse outcome of pregnancy. Pregnancy per se is a state of oxidative stress which is heightened in pregnancies complicated by diabetes, and the inflammation associated with preeclampsia and increasing maternal BMI. Both reactive oxygen and nitrogen species including superoxide and nitric oxide have roles in placental physiology including regulation of vascular reactivity and signaling. With inflammation and heightened oxidative stress increased production of these reactive species leads to their interaction to produce a more powerful pro-oxidant, peroxynitrite, that can covalently modify proteins by tyrosine nitration leading to either gain or loss of function. We have shown functional effects of protein nitration on vascular reactivity on the placenta and using  a proteomic approach found p38MAP kinase activity to be reduced following nitration. The potential for rapid and reversible nitration of many proteins in the placenta implies a potential regulatory role. The increasing inflammatory and pro-oxidative milieu seen with increasing BMI is associated with a switch from protein carbonylaton reactions towards protein nitration suggesting again potential changes on covalent modification of proteins and their functions. There is also a sexual dimorphic effect on placental function and pregnancy outcomes potentially mediated via inflammatory pathways.