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Titolo:
Deflazacort increases laminin expression and myogenic repair, and induces early persistent functional gain in mdx mouse muscular dystrophy
Autore:
Anderson, JE; Weber, M; Vargas, C;
Indirizzi:
Univ Manitoba, Dept Human Anat & Cell Biol, Winnipeg, MB R3E 0W3, Canada Univ Manitoba Winnipeg MB Canada R3E 0W3 ol, Winnipeg, MB R3E 0W3, Canada
Titolo Testata:
CELL TRANSPLANTATION
fascicolo: 4, volume: 9, anno: 2000,
pagine: 551 - 564
SICI:
0963-6897(200007/08)9:4<551:DILEAM>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
SKELETAL-MUSCLE REGENERATION; IN-VIVO; EXTRACELLULAR-MATRIX; EPITHELIAL-CELLS; TAURINE; PREDNISONE; DIAPHRAGM; MYOD; DIFFERENTIATION; DEFICIENT;
Keywords:
muscle regeneration; myogenin; satellite cell; c-met; laminin; bFGF;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
40
Recensione:
Indirizzi per estratti:
Indirizzo: Anderson, JE Univ Manitoba, Dept Human Anat & Cell Biol, 730 William Ave, Winnipeg, MB R3E 0W3, Canada Univ Manitoba 730 William Ave Winnipeg MB Canada R3E 0W3 nada
Citazione:
J.E. Anderson et al., "Deflazacort increases laminin expression and myogenic repair, and induces early persistent functional gain in mdx mouse muscular dystrophy", CELL TRANSP, 9(4), 2000, pp. 551-564

Abstract

Deflazacort slows the progress of Duchenne muscular dystrophy (DMD) with fewer side effects than prednisone. In mdx mice, deflazacort treatment augments repair and growth of new muscle fibers. We tested the hypothesis that deflazacort improves muscle function and promotes repair by increasing myogenic cell proliferation and fiber differentiation. mdx mice (3.5 weeks old) were treated with deflazacort (1.2 mg/kg) or vehicle for 4 weeks. Forelimb grip strength was measured. After 4 weeks, the right tibialis anterior muscle (TA) was crush injured to induce synchronous regeneration. DNA was labeled using different markers 24 and 2 h before collecting tissues 4 days after injury. The expression of creatine kinase (CK) isoforms, laminin-2 (merosin) mRNA and protein, and proliferation by myogenic cells were measured andsatellite cells were identified by immunolocalization of c-met receptor. Peak grip strength increased 15% within 10 days of treatment, and was maintained up to 6 weeks after the end of treatment in a second experiment. Expression of CK MM in the regenerating TA rose from 46% to 55% of total CK activity after deflazacort treatment. Satellite cells were more numerous and appeared earlier on new fibers, in concert with a threefold increase in proliferation by myogenin+ (but not MyoD+) myoblasts. alpha 2-laminin mRNA expression and protein increased 1.3-5.5-fold relative to MM CK in regenerating and dystrophic TA, respectively. These studies support the hypothesis that deflazacort promotes functional gains, myogenic differentiation, myoblast fusion, and laminin expression in regenerating dystrophic muscle. The potential to augment precursor specification, strength, and possible membrane stability may be useful in directing long-term benefits for DMD patients and short-term amplification of precursors prior to myoblast transfer.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 23/09/20 alle ore 12:53:23