Hubel Research Group
Principal Investigator:
Carl Hubel, PhD
The Hubel lab aims to understand the pathogenesis of the pregnancy disorder preeclampsia, and why women who have experienced preeclampsia are at heightened risk for developing heart disease in later life.
The current NICHD-funded Program Project is designed to investigate the mechanisms by which obese and overweight women are at increased risk of developing preeclampsia. The lab seeks to determine why some obese women will develop preeclampsia whereas most others will not. Importantly, there are compelling reasons to believe that the focus on obese women as a high-risk group will be informative about the mechanisms of preeclampsia in general. The lab is also studying whether related factors contribute to elevated cardiovascular risk in nonpregnant women with a history of preeclampsia.
Dr. Hubel is currently Program Director of the five-year, National Institute of Child Health and Human Development (NICHD)-sponsored Program Project (P01), “Mechanisms of preeclampsia: Impact of obesity.” He is the Principal Investigator of sub-project III, “Endothelial progenitor function in pregnancy: Impact of obesity,” and of the Administrative Core of the Program. In this capacity, Dr. Hubel leads the country's largest program studying the mechanisms of preeclampsia.
Lab Members
Ashley Myerski
B.S. Biology
Email
412-641-5374
Marlise Franise Synder
M.S. Microbiology
Email
412-641-6208
Hillary Tomaswick
Selected Publications
- Roberts JM & Hubel CA. Pregnancy: a screening test for later life cardiovascular disease. Womens Health Issues, 20(5):304-7, Sep. 2010.
- Luppi P, Powers RW, Verma V, Edmunds L, Plymire D, & Hubel CA. Maternal circulating CD34+VEGFR-2+ and CD133+VEGFT-2 + progenitor cells increase during normal pregnancy but are reduced in women with preeclampsia. Reprod Sci, 17(7):643-52, Jul. 2010.
- Robinson NJ, Minchell LJ, Myers JE, Hubel CA, & Crocker IP. A potential role for free fatty acids in the pathogenesis of preeclampsia. J Hypertens, 27(6):687-92, Jun. 2009.
- von Versen-Hoeynck FM, Hubel CA, Gallaher MJ, Gammill HS, & Powers RW. Plasma levels of inflammatory markers neopterin, sialic acid, and C-reactive protein in pregnancy and preeclampsia. Am J Hypertens, 22(6):687-92, Jun. 2009.
- Lin C, Rajakumar A, Plymire DA, Verma V, Markovic N, & Hubel CA. Maternal endothelial progenitor colony-forming units with macrophage characteristics are reduced in preeclampsia. Am J Hypertens, 22(9):1014-19, 2009.
- Bainbridge SA, Roberts JM, von Versen-Höynck F, Koch J, Edmunds L, & Hubel CA. Uric acid attenuates trophoblast invasion and integration into cell monolayers. Am J Physiol Cell Physiol, 297(2): C440-50, 2009.
- Gandley RE, Rohland J, Zhou Y, Shibata E, Harger GF, Rajakumar A, Kagan VE, Markovic N, & Hubel CA. Increased myeloperoxidase in the placenta and circulation of women with preeclampsia. Hypertension, 52(2):387-93, 2008.
- 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, 51(6):1499-505, 2008.
- 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, 49:612-17, 2007.
- Shibata E, Powers RW, Rajakumar A, von Versen-Höynck F, Gallaher MJ, Lykins DL, Roberts JM, & 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), 291(5):E1009-16, 2006.
- Ramirez RJJ, *Hubel CA, Novak J, DiCianno JR, Kagan VE, & Gandley RE. Moderate ascorbic acid deficiency increases myogenic reactivity of arteries from pregnant but not virgin ascorbate-dependent rats. (*co-first authors) Hypertension 47(3):454-60, 2006.
- Shibata E, Rajakumar A, Powers RW, Larkin RW, Gilmour C, Crombleholme WR, Ness RB, Roberts JM, & Hubel CA. Soluble fms-like tyrosine kinase 1 (sFlt-1) is increased in preeclampsia but not in small for gestational age pregnancies: Relationship to circulating placental growth factor (PlGF). J Clin Endocrinol Metab, 90:4895-4903, 2005.
- *Wolf M, *Hubel CA, Lam C, Sampson M, Ecker JL, Ness RB, Rajakumar A, Daftary A, Shakir ASM, Seely EW, Roberts JM, Sukhatme VK, Karumanchi SA, & Thadhani R. Preeclampsia and future cardiovascular disease: potential role of altered angiogenesis and insulin resistance. (*co-first authors) J Clin Endocrinol Metab, 89:6239-43, 2004.
- Ramirez RJ, Novak J, Gandley RE, Johnston TP, McLaughlin MK, & Hubel CA. Endothelial function and myogenic reactivity in small mesenteric arteries of hyperlipidemic pregnant rats. Am J Physiol, (Regulatory Integrative Comp Physiol) 281:R1330-37, 2001.