skip to content »

Section of Atherosclerosis

Houston, Texas

BCM faculty, staff and trainees are the heart of the organization.
Section of Atherosclerosis and Vascular Medicine
not shown on screen

Joel D. Morrisett, Ph.D.

Positions:

Professor of Medicine and Biochemistry/Molecular Biology

Contact Information:

Phone: 713-798-4164
Pager: 281-735-9766
Fax: 832-640-9037
E-mail: morriset@bcm.tmc.edu

Basic and Clinical Research Interests:

The current standard of care for carotid atherosclerosis involves statin therapy. Statins not only inhibit cholesterol biosynthesis, but exert favorable pleiotropic effects on the arterial wall. Previous studies suggest that this drug can cause early regression of carotid atherosclerotic plaques. One of the objectives of our research program is to elucidate the mechanism(s) by which these favorable conditions occur. This objective is being pursued through three different approaches. The first approach is to determine in candidates for sequential carotid endarterectomy (CEA) if short term statin therapy alters the composition or dimensions of the plaque as measured in vivo and ex vivo by high resolution 3T MRI and feature space analysis. A second approach is to determine in candidates for bilateral CEA if short term therapy causes changes in tissue expression of mRNA that encodes proteins that modulate inflammation, oxidation, lipid transport, calcification, proteolysis, or hemorrhage. Laser capture microdissection, oligonucleotide microarray analysis, and high throughpout in situ hybridization (GenePaint), and immunohistochemistry (ProteinPaint) are being used to examine CEA tissues that have and have not been exposed to statin treatment. A third approach is to determine in candidates for bilateral CEA if short term statin therapy produces changes in CEA tissue and/or plasma levels of proteins involved in processes leading to atherosclerosis. This approach is being pursued using mass spectral imaging and high sensitivity protein microarray analysis (PMA). Mapping specific genes and proteins onto the 2D surface of histologic cross sections of atherosclerotic arteries provides useful information about the distribution of these macromolecules and how they might interact in vivo. These pharmacogenomic and pharmacoproteomic approaches have great potential for addressing central mechanisms leading to atherosclerosis and for discriminating between tissues that have/ have not been exposed to the pleiotropic effects of statins and other interventions.

Selected Publications:

E-mail this page to a friend