This is the home page for Steve Schwartz' lab. 

LAB DISCUSSIONS:  QuickTopics Discussion

The central interest of my lab is in the molecular biology underlying two diseases: atherosclerosis and hypertension.

Our central interest in atherosclerosis is in the plaque macrophage. Recently, Tom Nhan,  a graduate student in the lab, discovered a very unusual pathway for death in  plaque macrophage. Based on studies we had done on a systematic model for plaque rupture in mouse lesions, we have suggested that this pathway may be critical to formation of the necrotic core of the plaque and to the way plaques rupture.
Our central interest in hypertension is in the molecular basis for arterial wall thickening.  This is based on very simple idea.  (for a slide show click here ) In order for blood pressure to be raised, physiologic models showed that the MASS of the arterial wall must be increased.  This mass, stimulated even by normal stimuli, will over respond, elevating resistance on pressure.  To accomplish this, the artery must have a specialized signaling system to maintain mass as needed to control flow and pressure.  Using array display, Larry Adams, a fellow in the lab, discovered a gene, RGS-5, that appears (based so far on structure and in vitro studies) to fit the hypothesis for a controller of arterial mass.
The third area of the lab's interest is in atheroscleroitc plaque smooth muscle monoclonality.  Dr. Schwartz' mentor, Earl Benditt demonstrated monoclonality 30 years ago.  Since the usual examples of monoclonality are neoplasms, Benditt's data upset the usual concept of atherosclerosis.  However, Chuck Murry, then a fellow in the Schwartz lab, established that monoclonality was real.  The critical issue is whether this clonality arises as a mutation or has a developmental lineage origin. Current work in this area has used arrays to identify the unique phenotype of the plaque smooth muscle cell.

Other Links:

• Current Research
• CV

CVB website:  http://uwcvb.org/