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Journal of Biomedicine and Biotechnology
Volume 2011 (2011), Article ID 235216, 9 pages
Research Article

Equal Force Recovery in Dysferlin-Deficient and Wild-Type Muscles Following Saponin Exposure

Department of Cell and Molecular Physiology, Stritch School of Medicine, Loyola University Medical Center, Maywood, IL 60153, USA

Received 28 April 2011; Revised 24 June 2011; Accepted 19 July 2011

Academic Editor: Robert J. Bloch

Copyright © 2011 Piming Zhao et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Dysferlin plays an important role in repairing membrane damage elicited by laser irradiation, and dysferlin deficiency causes muscular dystrophy and associated cardiomyopathy. Proteins such as perforin, complement component C9, and bacteria-derived cytolysins, as well as the natural detergent saponin, can form large pores on the cell membrane via complexation with cholesterol. However, it is not clear whether dysferlin plays a role in repairing membrane damage induced by pore-forming reagents. In this study, we observed that dysferlin-deficient muscles recovered the tetanic force production to the same extent as their WT counterparts following a 5-min saponin exposure (50 μg/mL). Interestingly, the slow soleus muscles recovered significantly better than the fast extensor digitorum longus (EDL) muscles. Our data suggest that dysferlin is unlikely involved in repairing saponin-induced membrane damage and that the slow muscle is more efficient than the fast muscle in repairing such damage.