of sarcoglycan, identified as the delta subunit, experienced severe muscular dystrophy with large areas of cardiac cell death. Campbell and other researchers in his lab determined that this disruption in the sarcoglycan complex upsets vascular function and causes injury in cardiac and skeletal muscles. This injury leads to cardiac complications, which exacerbate LGMD.

"A number of proteins in cardiac muscle have been shown to be involved in cardiomyopathy," Campbell said. "However, our study opens up a unique and important new avenue of research directed toward the involvement of the vascular smooth muscle sarcoglycan-sarcospan complex in the cause and progression of cardiomyopathy."

Now that Campbell's lab has identified the problem that leads to cardiomyopathy in patients with LGMD, the next step is to look at possible pharmacological treatments to prevent vascular smooth muscle dysfunction. Campbell also wants to investigate gene transfer as a way to repair the sarcoglycan complex in vascular smooth muscles and develop additional animal models to evaluate smooth muscle contributions to cardiomyopathy.

In addition to Campbell, the other two primary investigators of this most recent study included postdoctoral associates Ramon Coral-Vazquez, Ph.D., and Ronald D. Cohn, M.D., both members of Campbell's Howard Hughes Medical Institute lab team. Other UI collaborators included Joseph A. Hill, M.D., Ph.D., assistant professor of internal medicine; Robert M. Weiss, M.D., associate professor of internal medicine; Robin Davisson, Ph.D., assistant professor of anatomy and cell biology; Steve Moore, M.D., Ph.D., professor of pathology; and Roger Williamson, M.D., professor of obstetrics and gynecology.

In addition to support from the Howard Hughes Medical Institute, the Muscular Dystrophy Association also funded this research.

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Contact: Jennifer Cronin
jennifer-cronin@uiowa.edu
319-335-9917
University of Iowa
17-Aug-1999

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