Reduced muscle necrosis and long-term benefits in dystrophic mdx mice after cV1q (blockade of TNF) treatment

被引:70
作者
Radley, Hannah G. [1 ]
Davies, Marilyn J. [1 ]
Grounds, Miranda D. [1 ]
机构
[1] Univ Western Australia, Sch Anat & Human Biol, Perth, WA 6009, Australia
关键词
DMD; mdx mouse; TNF; myofibre necrosis; voluntary exercise;
D O I
10.1016/j.nmd.2007.11.002
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Tumour necrosis factor (TNF) is a potent inflammatory cytokine that appears to exacerbate damage of dystrophic muscle in vivo. The monoclonal murine specific antibody cV1q that specifically neutralises murine TNF demonstrated significant anti-inflammatory effects in dystrophic mdx mice. cV1q administration protected dystrophic skeletal myofibres against necrosis in both young and adult mdx mice and in adult mdx mice subjected to 48 h voluntary wheel exercise. Long-term studies (up to 90 days) in voluntarily exercised mdx mice showed beneficial effects of cV1q treatment with reduced histological evidence of myofibre damage and a striking decrease in serum creatine kinase levels. However, in the absence of exercise long-term cV1q treatment did not reduce necrosis or background pathology in mdx mice. An additional measure of well-being in the cV1q treated mice was that they ran significantly more than control mdx mice. (C) 2007 Elsevier B.V. All rights reserved.
引用
收藏
页码:227 / 238
页数:12
相关论文
共 57 条
[1]   Cardiac and skeletal muscle adaptations to voluntary wheel running in the mouse [J].
Allen, DL ;
Harrison, BC ;
Maass, AH ;
Bell, ML ;
Byrnes, WC ;
Leinwand, LA .
JOURNAL OF APPLIED PHYSIOLOGY, 2001, 90 (05) :1900-1908
[2]   Persistent and improved functional gain in mdx dystrophic mice after treatment with L-arginine and deflazacort [J].
Archer, Jonathan D. ;
Vargas, Cinthya C. ;
Anderson, Judy E. .
FASEB JOURNAL, 2006, 20 (02) :738-+
[3]  
Arend WP, 2002, J RHEUMATOL, V29, P16
[4]   QUANTITATION OF MUSCLE PRECURSOR CELL-ACTIVITY IN SKELETAL-MUSCLE BY NORTHERN ANALYSIS OF MYOD AND MYOGENIN EXPRESSION - APPLICATION TO DYSTROPHIC (MDX) MOUSE MUSCLE [J].
BEILHARZ, MW ;
LAREU, RR ;
GARRETT, KL ;
GROUNDS, MD ;
FLETCHER, S .
MOLECULAR AND CELLULAR NEUROSCIENCE, 1992, 3 (04) :326-331
[5]   Duchenne muscular dystrophy [J].
Biggar, WD .
PEDIATRICS IN REVIEW, 2006, 27 (03) :83-88
[6]   Function and genetics of dystrophin and dystrophin-related proteins in muscle [J].
Blake, DJ ;
Weir, A ;
Newey, SE ;
Davies, KE .
PHYSIOLOGICAL REVIEWS, 2002, 82 (02) :291-329
[7]   Nitric oxide release combined with nonsteroidal anti inflammatory activity prevents muscular dystrophy pathology and enhances stem cell therapy [J].
Brunelli, Silvia ;
Sciorati, Clara ;
D'Antona, Giuseppe ;
Innocenzi, Anna ;
Covarello, Diego ;
Galvez, Beatriz G. ;
Perrotta, Cristiana ;
Monopoli, Angela ;
Sanvito, Francesca ;
Bottinelli, Roberto ;
Ongini, Ennio ;
Cossu, Giulio ;
Clementi, Emilio .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2007, 104 (01) :264-269
[8]   Muscle fibers of mdx mice are more vulnerable to exercise than those of normal mice [J].
Brussee, V ;
Tardif, F ;
Tremblay, JP .
NEUROMUSCULAR DISORDERS, 1997, 7 (08) :487-492
[9]   X-CHROMOSOME-LINKED MUSCULAR-DYSTROPHY (MDX) IN THE MOUSE [J].
BULFIELD, G ;
SILLER, WG ;
WIGHT, PAL ;
MOORE, KJ .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA-BIOLOGICAL SCIENCES, 1984, 81 (04) :1189-1192
[10]   Administration of the non-steroidal anti-inflammatory drug ibuprofen increases macrophage concentrations but reduces necrosis during modified muscle use [J].
Cheung, EV ;
Tidball, JG .
INFLAMMATION RESEARCH, 2003, 52 (04) :170-176