RENO — Leading muscular dystrophy researcher Dean Burkin of the University of Nevada, Reno School of Medicine, summarizes the impact of a new protein therapeutic, MG53, for the treatment of Duchenne muscular dystrophy in an article published this week in Science Translational Medicine.

“This is a focus article in which we summarize the impact of MG53 protein therapy as a treatment option and discuss the increasing number of new protein therapeutics being developed for the muscular dystrophies,” Burkin said.

Approaches to treat Duchenne muscular dystrophy include gene replacement therapy, gene repair and myoblast cell transfer.

In a study on MG53 by Noah Weislander and colleagues, presented in the same issue of Science Translational Medicine, it was found that mice that lack MG53 developed progressive muscle weakness and exhibit defective muscle repair after exercise or injury, and that MG53 facilitates rapid membrane repair to prevent damage to normal muscle.

The study suggests that treatment in combination with other protein therapies such as Burkin’s laminin-111 therapy, are likely to have synergy as well for Duchenne and other muscular dystrophies.

Burkin’s published research on laminin-111, a naturally occurring protein, showed it is quickly picked up in the bloodstream of mice and prevents muscle damage, an important finding for Duchenne muscular dystrophy, the most common form of muscular dystrophy.

Burkin’s work, which is funded by the National Institutes of Health, has also been featured on the website ScienCentral. His work was published in the Proceedings of the National Academy of Sciences as well as the January 2009 edition of American Journal of Pathology.

For more information on Burkin and a link to his publications on PubMed visit www.medicine.nevada.edu/dept/pharmacology/faculty/burkin.html.