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Titolo:
A role for nitric oxide in muscle repair: Nitric oxide-mediated activationof muscle satellite cells
Autore:
Anderson, JE;
Indirizzi:
Univ Manitoba, Dept Human Anat & Cell Sci, Winnipeg, MB R3E 0W3, Canada Univ Manitoba Winnipeg MB Canada R3E 0W3 ci, Winnipeg, MB R3E 0W3, Canada
Titolo Testata:
MOLECULAR BIOLOGY OF THE CELL
fascicolo: 5, volume: 11, anno: 2000,
pagine: 1859 - 1874
SICI:
1059-1524(200005)11:5<1859:ARFNOI>2.0.ZU;2-L
Fonte:
ISI
Lingua:
ENG
Soggetto:
DUCHENNE MUSCULAR-DYSTROPHY; ADULT SKELETAL-MUSCLE; RAT SOLEUS MUSCLE; ENDOTHELIAL-CELLS; GENE-EXPRESSION; TELOMERE LENGTH; SYNTHASE GENE; SHEAR-STRESS; LIMB MUSCLE; MYOD FAMILY;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
110
Recensione:
Indirizzi per estratti:
Indirizzo: Anderson, JE Univ Manitoba, Dept Human Anat & Cell Sci, Winnipeg, MB R3E 0W3, Canada Univ Manitoba Winnipeg MB Canada R3E 0W3 MB R3E 0W3, Canada
Citazione:
J.E. Anderson, "A role for nitric oxide in muscle repair: Nitric oxide-mediated activationof muscle satellite cells", MOL BIOL CE, 11(5), 2000, pp. 1859-1874

Abstract

Muscle satellite cells are quiescent precursors interposed between myofibers and a sheath of external lamina. Although their activation and recruitment to cycle enable muscle repair and adaptation, the activation signal is not known. Evidence is presented that nitric oxide (NO) mediates satellite cell activation, including morphological hypertrophy and decreased adhesion in the fiber-lamina complex. Activation in vivo occurred within 1 min afterinjury. Cell isolation and histology showed that pharmacological inhibition of nitric oxide synthase (NOS) activity prevented the immediate injury-induced myogenic cell release and delayed the hypertrophy of satellite cells in that muscle. Transient activation of satellite cells in contralateral muscles 10 min later suggested that a circulating factor may interact with NO-mediated signaling. Interestingly, satellite cell activation in muscles ofmdx dystrophic mice and NOS-I knockout mice quantitatively resembled NOS-inhibited release of normal cells, in agreement with reports of displaced and reduced NOS expression in dystrophin-deficient mdx muscle and the complete loss of NOS-I expression in knockout mice. Brief NOS inhibition in normaland mdx mice during injury produced subtle alterations in subsequent repair, including apoptosis in myotube nuclei and myotube formation inside laminar sheaths. Longer NOS inhibition delayed and restricted the extent of repair and resulted in fiber branching. A model proposes the hypothesis that NOrelease mediates satellite cell activation, possibly via shear-induced rapid increases in NOS activity that produce "NO transients".

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/09/20 alle ore 23:38:16