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Titolo:
Sublytic C5b-9-stimulated Schwann cell survival through PI 3-kinase-mediated phosphorylation of BAD
Autore:
Hila, S; Soane, L; Koski, CL;
Indirizzi:
Univ Maryland, Sch Med, Dept Neurol, Baltimore, MD 21201 USA Univ Maryland Baltimore MD USA 21201 Dept Neurol, Baltimore, MD 21201 USA Univ Maryland, Sch Med, Dept Pathol, Baltimore, MD 21201 USA Univ Maryland Baltimore MD USA 21201 Dept Pathol, Baltimore, MD 21201 USA
Titolo Testata:
GLIA
fascicolo: 1, volume: 36, anno: 2001,
pagine: 58 - 67
SICI:
0894-1491(200110)36:1<58:SCSCST>2.0.ZU;2-W
Fonte:
ISI
Lingua:
ENG
Soggetto:
TERMINAL COMPLEMENT COMPLEXES; ACTIVATED PROTEIN-KINASE; GUILLAIN-BARRE-SYNDROME; PERIPHERAL NERVOUS-SYSTEM; GROWTH-FACTOR-I; PHOSPHATIDYLINOSITOL 3-KINASE; SYMPATHETIC NEURONS; MEDIATED APOPTOSIS; SIGNALING PATHWAY; GLIAL-CELLS;
Keywords:
glial cells; apoptosis; complement; Akt, Bcl-x(L);
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
60
Recensione:
Indirizzi per estratti:
Indirizzo: Koski, CL Univ Maryland Hosp, Dept Neurol, Room N4W46,22 S Greene St, Baltimore, MD 21201 USA Univ Maryland Hosp Room N4W46,22 S Greene St Baltimore MD USA 21201
Citazione:
S. Hila et al., "Sublytic C5b-9-stimulated Schwann cell survival through PI 3-kinase-mediated phosphorylation of BAD", GLIA, 36(1), 2001, pp. 58-67

Abstract

Sublytic C5b-9 induces cell cycle activation, proliferation, and rescue from apoptosis in Schwann cells. The signaling pathways for C5b-9-mediated rescue were investigated. Following serum withdrawal, DNA fragmentation, detected by TUNEL and FAGS analysis, was 56.7% +/- 7.3 and 91.9% +/- 2.4 in cultured sciatic nerve Schwann cells from 6-day-old rats after 18 h and 24 h, respectively. Apoptosis was confirmed by inhibition of DNA fragmentation ina dose-dependent manner by DMQD-CHO, a caspase-3 inhibitor. Treatment withsublytic C5b-9 generated with purified components (C5*9) or Ab+C7-depletedserum (C7dHS)+C7 rescued 89% and 86% of Schwann cells, respectively, as compared with cells treated with C5*6, C8, C9, or Ab+C7dHS. Sublytic C5b-9 increased Schwann cell PI-3 kinase and Akt activity maximally at 5 min 3.14 +/- 0.5-fold and 3.56 +/- 0.4-fold, respectively, over controls. ERK-1 activity was maximally stimulated 2.98-fold at 15 min. Inhibition of PI-3 kinaseby LY294002 abrogated the C5b-9-mediated Schwann cell rescue from apoptosis, while inhibition of ERK-1 with PD098,059 did not. PI-3 kinase-Akt pathway activation by C5b-9 induced, within 15 min, a 6.34 +/- 1.2-fold increase in BAD phosphorylation at Ser 136, but not at Ser 112. Downstream Bcl-x(L) protein was increased 2.61-fold +/- 0.34-fold by 18 h and 3.9-fold +/- 0.84-fold by 24 h over controls. LY294002 prevented both BAD phosphorylation atSer 136 and Bcl-x(L) protein induction, while PD098,059 did not. Our data indicated that sublytic C5b-9 rescued Schwann cell from apoptosis via activation of PI-3 kinase-Akt, BAD phosphorylation on Ser 136 and increased expression of Bcl-x(L). Sublytic C5b-9 detected on Schwann cell in vivo during inflammatory neuropathy may facilitate survival of Schwann cell capable of remyelination. (C) 2001 Wiley-Liss, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 27/09/20 alle ore 06:27:38