Francis Miller, Jr., M.D. (Full Member)
Associate Professor, Internal Medicine, University of Iowa

http://www.int-med.uiowa.edu/Divisions/Cardiology/Directory/FrancisMiller.html

Research Interest    

Dr. Miller's research focuses on the role of reactive oxygen species in vascular disease, the central goal being to understand the molecular and cellular mechanisms that contribute to the generation of reactive oxygen species and to the pathophysiology of vascular disease. Such an understanding may lead to the development of new strategies for the treatment of hypertension, atherosclerosis, and stroke. Ongoing studies are examining: (1) the regulation and function of NADPH oxidases - Nox1 and Nox4 in particular - in vascular smooth muscle cells; (2) the role of the antiporter ClC-3, which is emerging as a novel and essential component of Nox-dependent redox-mediated cell signaling, in vascular cell physiology; (3) the physiologic importance of increased levels of reactive oxygen species in the vascular response to injury. Experimental approaches include the use of murine models in which free radical generation and metabolism are altered, as well as murine models of atherosclerosis and carotid injury. Studies in vascular physiology and cellular biology examine gene expression and regulation, protein function, the generation of reactive oxygen species, redox-mediated signaling, and vascular cell migration and proliferation. Where applicable, the findings are extended to include the study of human vascular disease.

Selected Publications:

Hathaway, C.A., Heistad, D.D., Piegors, D.J., and Miller, Jr., F.J.: Regression of atherosclerosis in monkeys reduces vascular superoxide levels. Circ. Res. 90:277-283, 2002.

Miller, F.J. Jr., Filali M, Huss GJ, Stanic B, Chamseddine A, Barna TJ, and Lamb FS. Cytokine activation of NF-kB in vascular smooth muscle cells requires signaling endosomes containing Nox1 and ClC-3. Circulation Research, 101:663-671, 2007.

Jagadeesha DK, Miller, F.J. Jr., Bhalla RC. Inhibition of apoptotic signaling and neointimal hyperplasia by tempol and nitric oxide synthase following vascular injury. J Vascular Research, 46;109-18, 2008.

Miller, F.J. Jr., Chu X., Stanic B., Tian X., Sharma R.V., Davisson R.L., Lamb F.S. A differential role for endocytosis in receptor-mediated activation of Nox1. Antioxid Redox Signal, in press, 2009.

Publications from Gene Therapy Center

Publications from PubMed