Am J Physiol Cell Physiol Journal of Applied Physiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Cell Physiol 294: C1183-C1191, 2008. First published March 19, 2008; doi:10.1152/ajpcell.00568.2007
0363-6143/08 $8.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
294/5/C1183    most recent
00568.2007v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Cheng, M.
Right arrow Articles by Koh, T. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Cheng, M.
Right arrow Articles by Koh, T. J.

MUSCLE CELL BIOLOGY AND CELL MOTILITY

Endogenous interferon-{gamma} is required for efficient skeletal muscle regeneration

Ming Cheng, Mai-Huong Nguyen, Giamila Fantuzzi, and Timothy J. Koh

Department of Kinesiology and Nutrition, University of Illinois at Chicago, Chicago, Illinois

Submitted 29 November 2007 ; accepted in final form 14 March 2008

The inflammatory response is thought to play important roles in tissue healing. The hypothesis of this study was that the inflammatory cytokine interferon (IFN)-{gamma} is produced endogenously following skeletal muscle injury and promotes efficient healing. We show that IFN-{gamma} is expressed at both mRNA and protein levels in skeletal muscle following injury, and that the time course of IFN-{gamma} expression correlated with the accumulation of macrophages, T-cells, and natural killer cells, as well as myoblasts, in damaged muscle. Cells of each type were isolated from injured muscle, and IFN-{gamma} expression was detected in each cell type. We also demonstrate that administration of an IFN-{gamma} receptor blocking antibody to wild-type mice impaired induction of interferon response factor-1, reduced cell proliferation, and decreased formation of regenerating fibers. IFN-{gamma} null mice showed similarly impaired muscle healing associated with impaired macrophage function and development of fibrosis. In vitro studies demonstrated that IFN-{gamma} and its receptor are expressed in the C2C12 muscle cell line, and that the IFN-{gamma} receptor blocking antibody reduced proliferation and fusion of these muscle cells. In summary, our results indicate that IFN-{gamma} promotes muscle healing, in part, by stimulating formation of new muscle fibers.

cytokine; inflammation; macrophage; tissue repair



Address for reprint requests and other correspondence: T. J. Koh, Dept. of Kinesiology and Nutrition, Univ. of Illinois at Chicago, 1919 W. Taylor, Rm. 529 m/c 994, Chicago, IL 60612 (e-mail: tjkoh{at}uic.edu)







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2008 by the American Physiological Society.