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Titolo:
Microglia at brain stab wounds express connexin 43 and in vitro form functional gap junctions after treatment with interferon-gamma and tumor necrosis factor-alpha
Autore:
Eugenin, EA; Eckardt, D; Theis, M; Willecke, K; Bennett, MVL; Saez, JC;
Indirizzi:
Pontificia Univ Catolica Chile, Fac Ciencias Biol, Dept Ciencias Fisiol, Santiago 340, Chile Pontificia Univ Catolica Chile Santiago Chile 340 l, Santiago 340, Chile Univ Bonn, Genet Inst, D-53117 Bonn, Germany Univ Bonn Bonn Germany D-53117 v Bonn, Genet Inst, D-53117 Bonn, Germany Yeshiva Univ Albert Einstein Coll Med, Dept Neurosci, Bronx, NY 10461 USA Yeshiva Univ Albert Einstein Coll Med Bronx NY USA 10461 nx, NY 10461 USA
Titolo Testata:
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
fascicolo: 7, volume: 98, anno: 2001,
pagine: 4190 - 4195
SICI:
0027-8424(20010327)98:7<4190:MABSWE>2.0.ZU;2-B
Fonte:
ISI
Lingua:
ENG
Soggetto:
CENTRAL-NERVOUS-SYSTEM; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; MESSENGER-RNA EXPRESSION; RAT-LIVER; PROTEIN CONNEXIN-43; MULTIPLE-SCLEROSIS; MURINE MACROPHAGES; REACTIVE MICROGLIA; ALZHEIMERS-DISEASE; GROWTH-FACTOR;
Keywords:
inflammation; macrophage; connexin; cytokines; dye coupling;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
45
Recensione:
Indirizzi per estratti:
Indirizzo: Saez, JC Pontificia Univ Catolica Chile, Fac Ciencias Biol, Dept Ciencias Fisiol, Alameda 340, Santiago 340, Chile Pontificia Univ Catolica Chile Alameda 340 Santiago Chile 340 le
Citazione:
E.A. Eugenin et al., "Microglia at brain stab wounds express connexin 43 and in vitro form functional gap junctions after treatment with interferon-gamma and tumor necrosis factor-alpha", P NAS US, 98(7), 2001, pp. 4190-4195

Abstract

Gap junctional communication between microglia was investigated at rat brain stab wounds and in primary cultures of rat and mouse cells. Under resting conditions, rat microglia (FITC-isolectin-B4-reactive cells) were sparsely distributed in the neocortex, and most (95%) were not immunoreactive for Cx43, a gap junction protein subunit. At brain stab wounds, microglia progressively accumulated over several days and formed aggregates that frequently showed Cx43 immunoreactivity at interfaces between cells. In primary culture, microglia showed low levels of Cx43 determined by Western blotting, diffuse intracellular Cx43 immunoreactivity, and a low incidence of dye coupling. Treatment with the immunostimulant bacterial lipopolysaccharide (LPS) or the cytokines interferon-gamma (INF-gamma) or tumor necrosis factor-alpha (TNF-alpha) one at a time did not increase the incidence of dye coupling. However, microglia treated with INF-gamma plus LPS showed a dramatic increase in dye coupling that was prevented by coapplication of an anti-TNF-alpha antibody, suggesting the release and autocrine action of TNF-alpha. Treatment with INF-gamma plus TNF-alpha also greatly increased the incidence of dye coupling and the Cx43 levels with translocation of Cx43 to cell-cell contacts. The cytokine-induced dye coupling was reversibly inhibited by 18 alpha -glycyrrhetinic acid, a gap junction blocker. Cultured mouse microglia also expressed Cx43 and developed dye coupling upon treatment with cytokines, but microglia from homozygous Cx43-deficient mice did not develop significant dye coupling after treatment with either INF-gamma plus LPS or INF-gamma plus TNF-alpha. This report demonstrates that microglia can communicatewith each other through gap junctions that are induced by inflammatory cytokines, a process that may be important in the elaboration of the inflammatory response.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 09/07/20 alle ore 17:26:43