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Titolo:
Tumor necrosis factor alpha and human Schwann cells: Signalling and phenotype modulation without cell death
Autore:
Bonetti, B; Valdo, P; Stegagno, C; Tanel, R; Zanusso, G; Ramarli, D; Fiorini, E; Turazzi, S; Carner, M; Moretto, G;
Indirizzi:
Univ Verona, Sez Neurol Clin, I-37100 Verona, Italy Univ Verona Verona Italy I-37100 Sez Neurol Clin, I-37100 Verona, Italy Univ Verona, Dipartimento Sci Neurol & Vis, Sez Neurochirurg, I-37100 Verona, Italy Univ Verona Verona Italy I-37100 Sez Neurochirurg, I-37100 Verona, Italy Univ Verona, Dipartimento Patol, Sez Immunol, I-37100 Verona, Italy Univ Verona Verona Italy I-37100 tol, Sez Immunol, I-37100 Verona, Italy Univ Verona, Ist Otorinolaringoiatria, I-37100 Verona, Italy Univ Verona Verona Italy I-37100 inolaringoiatria, I-37100 Verona, Italy Azienda Ospedaliera, Serv Immunol, Verona, Italy Azienda Ospedaliera Verona Italy pedaliera, Serv Immunol, Verona, Italy
Titolo Testata:
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY
fascicolo: 1, volume: 59, anno: 2000,
pagine: 74 - 84
SICI:
0022-3069(200001)59:1<74:TNFAAH>2.0.ZU;2-7
Fonte:
ISI
Lingua:
ENG
Soggetto:
NF-KAPPA-B; MYELIN-ASSOCIATED GLYCOPROTEIN; TNF-ALPHA; TRANSCRIPTION FACTOR; SODIUM-SALICYLATE; INDUCED APOPTOSIS; FACTOR RECEPTORS; EXPRESSION; ACTIVATION; PROLIFERATION;
Keywords:
c-jun; de-differentiation; NF kappa B; NGF receptor; Schwann cells; TNF alpha; transcription factors;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
42
Recensione:
Indirizzi per estratti:
Indirizzo: Bonetti, B Univ Verona, Policlin Borgo Roma, Ist Neurol, I-37134 Verona, Italy Univ Verona Verona Italy I-37134 eurol, I-37134 Verona, Italy
Citazione:
B. Bonetti et al., "Tumor necrosis factor alpha and human Schwann cells: Signalling and phenotype modulation without cell death", J NE EXP NE, 59(1), 2000, pp. 74-84

Abstract

The aim of the study was to evaluate the biological response of human Schwann cells (SC) to turner necrosis factor alpha (TNF alpha) in vitro and to the inflammatory milieu of chronic inflammatory demyelinating polyradiculoneuritis (CIDP). By immunocytochemical and functional assays, we found that SC expressed TNF receptors and that TNF alpha promoted in SC cultures transient activation of transcription factors NF kappa B and c-jun in the absence of apoptosis. In addition, TNF alpha significantly increased the proportion of non-myelin-forming SC expressing the p75 nerve growth factor receptor. Such phenotypic effect was dose-dependent and partially mediated by NF kappa B, as assessed by functional blockage with acetylsalicylic acid. We then extended our study to a human disease in which SC are exposed to TNF alpha. Increased signals for NF kappa B, but not c-jun, molecules were observedby immunohistochemistry on SC nuclei in nerve biopsies from patients with CIDP, as compared with controls. Irrespective of the presence of nerve inflammation, SC showed no evidence of apoptosis. Taken together, our results suggested that SC are potential targets of TNF alpha and that this cytokine exerted no cytotoxic effects either in vivo or in vitro. Rather, TNF alpha may influence the fate of SC by activating transcriptional pathways and modulating their phenotype.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 09/07/20 alle ore 13:48:23