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Robert W. Powers, Ph.D.
Assistant Investigator, Magee-Womens Research Institute
Assistant Professor, Obstetrics, Gynecology and Reproductive Sciences, University of Pittsburgh
Ph.D., University of Cincinnati, College of Medicine, 1996
Postdoctoral Fellowship, Magee-Womens Research Institute, 1996-2000
Research Interests
Dr. Powers is currently working on two main projects in the laboratory, and both are related to the pregnancy complication, preeclampsia. Preeclampsia is a specific hypertensive disorder of pregnancy and is a major cause of both maternal and fetal morbidity and mortality, contributing significantly to preterm birth and fetal growth restriction. The underlying cause of preeclampsia is unknown, however several pre-existing conditions increase the risk of preeclampsia including obesity. Since obesity is very prevalent in the US population (30% of adults), obesity is likely the single most significant risk factor for preeclampsia accounting for between 15-32% of all cases. One project in the lab is investigating the role of asymmetric dimethylarginine (ADMA) as one mechanism by which obesity increases the risk of preeclampsia. ADMA is an endogenous inhibitor of nitric oxide synthase (NOS). High ADMA contributes to endothelial dysfunction and inhibits angiogenesis and arteriogenesis (activities important in pregnancy and deficient in preeclampsia). ADMA is higher in obesity, and it is higher early in pregnancy among women who later develop preeclampsia. The second project in the lab is investigating differences in amino acid concentrations and transport in preeclampsia and fetal growth restriction. Amino acids are critical in fetal growth and development, and the fetus is almost entirely dependent upon maternal sources of amino acids. We have previously described important differences in amino acid concentrations and placental transport in pregnancies with and without growth restricted infants in the presence and absence of preeclampsia.
Selected Publications
Powers RW, Majors AK, Kerchner LJ, Conrad KP. Renal handling of maternal homocysteine during normal pregnancy and preeclampsia. J Soc Gynecol Invest, 11(1):45-50, 2004.
Powers RW, Gandley RE, Lykins DL, Roberts JM. Moderate hyperhomocysteinemia decreases endothelial-dependent vasorelaxation in pregnant but not nonpregnant mice. Hypertension, 44:327-333, 2004.
Powers RW, Roberts JM, Cooper KM, Gallaher MJ, Frank MP, Harger GF, Ness RB. Maternal serum sFlt-1 concentrations are not increased in early pregnancy and decrease more slowly postpartum in women who develop preeclampsia. Am J Obstet Gynecol, 193:185-191, 2005.
Roberts JM, Bodnar LM. Lain KY, Hubel CA, Markovic N, Ness RB, Powers RW. Uric acid is as important as proteinuria in identifying fetal risk in women with gestational hypertension. Hypertension, 46:1263-1269, 2005.
Powers RW, Bodnar LM, Ness RB, Cooper KM, Gallaher MJ, Frank MP, Daftary AR, Roberts JM. Uric acid concentrations are increased throughout pregnancy among women with gestational hyperuricemia at delivery. Am J Obstet Gynecol, 194:161-168, 2006.
Shibata E, Hubel CA, Powers RW, Rajakumar A, Gallaher MJ, Roberts JM. Angiotensin II (ANGII) Type I Receptor (AT1-R) activation reduces system A amino acid transport in human placental villi. J Clin Endo Metab, 2006, accepted for publication.
Professional Affiliations
American Association for the Advancement of Science
Society for the Study of Reproduction
International Society for the Study of Hypertension in Pregnancy
The American Physiological Society
The Society for Gynecologic Investigation
The North American Society for the Study of Hypertension in Pregnancy (Secretary/Treasurer 2006-2008)
Contact Information
Magee-Womens Research Institute
204 Craft Avenue
Pittsburgh, PA 15213
Telephone: (412) 641-6005
Fax: (412) 641-1503
e-mail: rsirwp@mwri.magee.edu
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