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Scavenger receptor mRNAs in rat brain microglia are induced by kainic acid lesioning and by cytokines.
Grewal, R P; Yoshida, T; Finch, C E; Morgan, T E.
  • Grewal RP; Department of Neurology, School of Medicine, University of Southern California, Los Angeles 90089-0191, USA.
Neuroreport ; 8(5): 1077-81, 1997 Mar 24.
Article en En | MEDLINE | ID: mdl-9175088
The expression and localization of two distinct mRNAs from the macrophage scavenger receptor gene family were studied in rat brain cells in vivo and in vitro. In general, brains of control male rats showed low level signals by in situ hybridization for the macrophage scavenger receptor (MSR) and murine adherent macrophage (MAMA) receptor. In contrast, the reticular thalamic nucleus had a subpopulation of intensely labeled cells. Kainic acid (KA) treatment induced MSR and MAMA mRNA levels on different schedules in brain regions that are susceptible to KA, including hippocampal areas CA1 and CA3. The combination of immunocytochemistry and in situ hybridization localized the MSR and MAMA mRNA to microglia of KA-treated rats. Northern blot hybridization detected both MSR and MAMA mRNAs in primary cultures of mixed glia that contained microglia. Both MSR and MAMA mRNA were induced by treatment of primary mixed glia with lipopolysaccharide and interferon-gamma, but not TGF beta 1. MSR, but not MAMA, mRNA levels were increased after treatment with interleukin-1 alpha. These results demonstrate the differential regulation of scavenger receptor mRNAs in microglia that is consistent with distinct roles for scavenger receptors in responses to neurodegeneration.
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Banco de datos: MEDLINE Asunto principal: Encéfalo / ARN Mensajero / Receptores Inmunológicos / Moléculas de Adhesión Celular / Citocinas / Microglía Límite: Animals Idioma: En Año: 1997 Tipo del documento: Article
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Banco de datos: MEDLINE Asunto principal: Encéfalo / ARN Mensajero / Receptores Inmunológicos / Moléculas de Adhesión Celular / Citocinas / Microglía Límite: Animals Idioma: En Año: 1997 Tipo del documento: Article