Pathology

Gary Baumbach, MD

Portrait

Mailing Address

Office: 5231D RCP
Iowa City, IA 52242
Phone: +1 319 384 9083
Email: g-baumbach@uiowa.edu

Web: Research Laboratory (Structure and Function of Cerebral Blood Vessels)

Education

BA, Wartburg College, 1971
Externship, Pathology, University of Iowa Hospitals and Clinics, 1975
MD, Medicine, University of Iowa College of Medicine, 1976
Residency, Pathology, University of Iowa Hospitals and Clinics, 1977
Residency, Ophthalmology, University of Iowa Hospitals and Clinics, 1980
Fellowship, Cardiovascular/Neuropathology, University of Iowa Hospitals and Clinics, 1981
Fellowship, Neuropathology, University of Iowa Hospitals and Clinics, 1984

Appointments

Primary: Pathology

Center and Program Affiliations

  • Interdisciplinary Graduate Program in Informatics

Research Interests

aging, brain tumor, diabetes, pathophysiology in hypertension, vascular biology

Research Summary

The long-term objective of studies in our laboratory is to clarify the relationship between morphology and function of blood vessels in the brain, and to understand the influence of structural changes produced by chronic hypertension and aging on function of the vessel wall. To achieve these goals, in vivo and in vitro methods are used to analyze cerebral vascular mechanics, and morphometric methods to quantitate components of the vessel wall. Hypotheses that are currently being tested include: 1) that contraction of smooth muscle in cerebral arterioles is augmented in early hypertension, prior to the development of vascular hypertrophy, and contraction may be affected by structural alterations that develop during prolonged hypertension, 2) that effects of chronic hypertension on smooth muscle contraction may be different with respect to vessel size and brain region, and 3) that effects of aging on structure and function of blood vessels in the brain may be similar, in some respects, to effects of chronic hypertension. In addition to these interests, our laboratory has recently undertaken a new direction with the aim of extending studies of vascular mechanics and structure to the cellular level. Initial efforts have focused on the use of confocal microscopy and computer-assisted image analysis to examine effects of mechanical deformation on focal and near contacts (focal adhesion sites) in vascular smooth muscle in tissue culture. Focal contacts provide anchorage sites essential for the maintenance of tension within the cell, and are involved in regulation of cell morphology, proliferation, migration, differentiation and responsiveness. It is anticipated that these studies will lead to greater understanding of the fundamental mechanisms that are involved in structural changes in the vessel wall as related to increases in mechanical stress that accompany chronic hypertension and aging.

Publications

  • Rodionov, R, Dayoub, H, Lynch, C, Wilson, K, Stevens, J, Murry, D, Kimoto, M, Arning, E, Bottiglieri, T, Cooke, J, Baumbach, G, Faraci, F, Lentz, S. Overexpression of dimethylarginine dimethylaminohydrolase protects against cerebral vascular effects of hyperhomocysteinemia. Circ Res 106(3):551-8, 2010. [PubMed]
  • Grigoryan, M, Geisler, S, St Louis, E, Baumbach, G, Davis, P. Cerebral arteriolar thromboembolism in idiopathic hypereosinophilic syndrome. Arch Neurol 66(4):528-31, 2009. [PubMed]
  • Wakisaka, Y, Miller, JD, Chu, Y, Baumbach, GL, Wilson, S, Faraci, FM, Sigmund, CD, Sigmund, CD, Sigmund, CD, Heistad, DD. Activation of NAD(P)H oxidase and oxidative stress precede spontaneous intracranial hemorrhage in hypertensive mice. STROKE 39(2):653-653, FEB 2008.
  • Halabi, C, Beyer, A, de Lange, W, Keen, H, Baumbach, G, Faraci, F, Sigmund, C. Interference with PPAR gamma function in smooth muscle causes vascular dysfunction and hypertension. Cell Metab 7(3):215-26, 2008. [PubMed]
  • Wakisaka, Y, Miller, J, Chu, Y, Baumbach, G, Wilson, S, Faraci, F, Sigmund, C, Heistad, D. Oxidative stress through activation of NAD(P)H oxidase in hypertensive mice with spontaneous intracranial hemorrhage. J Cereb Blood Flow Metab 28(6):1175-85, 2008. [PubMed]
  • Beyer, A, Baumbach, G, Halabi, C, Modrick, M, Lynch, C, Gerhold, T, Ghoneim, S, de Lange, W, Keen, H, Tsai, Y, Maeda, N, Sigmund, C, Faraci, F. Interference with PPARgamma signaling causes cerebral vascular dysfunction, hypertrophy, and remodeling. Hypertension 51(4):867-71, 2008. [PubMed]
  • Baumbach, G, Didion, S, Faraci, F. Hypertrophy of cerebral arterioles in mice deficient in expression of the gene for CuZn superoxide dismutase. Stroke 37(7):1850-5, 2006. [PubMed]
  • Iida, S, Baumbach, G, Lavoie, J, Faraci, F, Sigmund, C, Heistad, D. Spontaneous stroke in a genetic model of hypertension in mice. Stroke 36(6):1253-8, 2005. [PubMed]
  • Didion SP, Lynch CM, Baumbach GL, Faraci FM.  Impaired endothelium-dependent responses and enhanced influence of Rho-kinase in cerebral arterioles in Type II diabetes.  Stroke.  36:342-347, 2005.
  • Didion SP, Lynch CM, Baumbach GL, Faraci FM.  Impaired endothelium-dependent responses and enhanced influence of Rho-kinase in cerebral arterioles in Type II diabetes.  Stroke.  36:342-347, 2005.