Carl A. Hubel, PhD
Associate Professor, Department of Obstetrics, Gynecology & Reproductive Sciences, School of Medicine, University of Pittsburgh
Globally, preeclampsia and other hypertensive disorders of pregnancy are a leading cause of maternal and infant illness and death. I am seeking to better understand what causes preeclampsia. I am also researching why it is that women with a history of preeclampsia or related pregnancy disorders are at higher risk of developing hypertension, heart disease or stroke when they become older. My research team is testing to see if stress signals from pregnancy, as may be measured in blood or urine, or by looking for abnormalities in the placenta, can help identify heart disease risk in women and unravel the the causes.
Carl A. Hubel, PhD
Research in Brief
The “Pregnancy Adaptation” research team led by Dr. Hubel is currently funded by the American Heart Association as a Center within the Go Red For Women Strategically Focused Research Network (SFRN). The theme of the overall Center is “Women’s Cardiovascular Health and Microvascular Mechanisms: Novel Insights from Pregnancy”. Women with adverse pregnancy outcomes, including preeclampsia, preterm delivery or intrauterine growth restriction, have a significantly (2- to 8-fold) increased risk of hypertension, coronary artery disease or stroke in the years after delivery. Pregnancy is thus a natural “stress test” that may reveal risk of later CVD. The Magee Go Red Center posits that individual differences in a woman’s cardiovascular and metabolic (cardiometabolic) response to the challenge of pregnancy can provide valuable and unique information about her future health and, further, that this information can be utilized to delineate differing trajectories over the ensuing decades, be that continued freedom from CVD or accelerating cardiometabolic dysfunction. Here an important goal is to identify mechanisms of later life CVD in women that are unmasked by pregnancy phenotype including maladaptive vascular responses to pregnancy and placental pathology. In addition to his role as center Director, Dr. Hubel is also PI of the Clinical Project, “Glycocalyx Pathways Linking Pregnancy Profile with Microvascular Dysfunction Postpartum”. In this context, his clinical team is testing the hypothesis that damage to the vascular endothelial glycocalyx (endothelial surface layer) underlies development of both the maternal manifestations of preeclampsia and later-life CVD, and thus is a potential target for therapy.
- Mosca L, Ouyang P, Hubel C, Reynolds H, Allison M. Go Red for Women Strategically Focused Research Network (SFRN) Centers. Circulation. 2017;135:609-611.
- Hubel CA, Griggs KC, McLaughlin MK. Lipid peroxidation and altered vascular function in vitamin E-deficient rats. Am J Physiol. 1989;256 (Heart Circ Physiol 25):H1539-1545.
- Shibata E, Powers RW, Rajakumar A, von Versen-Höynck F, Gallaher MJ, Lykins DL, Roberts JM and Hubel CA. Angiotensin II decreases system A amino acid transporter activity in human placental villous fragments through AT1 receptor activation. Am J
Physiol Endocrinol Metab. 2006;291:E1009-1016.
- Bainbridge SA, Roberts JM, von Versen-Höynck F, Koch J, Hubel CA. Uric acid attenuates trophoblast invasion and integration into endothelial cell monolayers. Am J Physiol Cell Physiol. 2009;297:C440-450.
- Hubel CA, Wallukat G, Wolf M, Herse F, Rajakumar A, Roberts JM, Markovic N, Thadhani R, Luft FC, Dechend R. Agonistic AT1-receptor autoantibodies in post-partum women with a history of preeclampsia. Hypertension. 2007;49:612-617.
- Hubel CA, Powers RW, Sneadal S, Gammill HS, Ness RB, Roberts JM, Arngrimsson R. C-reactive protein is elevated 30 years after eclamptic pregnancy. Hypertension. 2008;51:1499-1505.
- von Versen-Höynck F, Brodowski L, Dechend R, Myerski AC, Hubel CA. Vitamin D antagonizes negative effects of preeclampsia on fetal endothelial colony forming cell number and function. PLoS One. 2014; 9(6):e98990.
- Weissgerber TL, Rajakumar A, Myerski A, Edmunds LR, Powers RW, Roberts JM, Gandley RE, Hubel CA. Vascular pool of releasable soluble VEGF receptor-1 (sFLT1) in women with previous preeclampsia and uncomplicated pregnancy. J Clin Endocrinol Metab. 2014;99:978-987.
For additional publications, visit Pubmed.