Complement and cytokine gene expression in cultured microglia derived from postmortem human brains
Identifieur interne : 004059 ( Main/Exploration ); précédent : 004058; suivant : 004060Complement and cytokine gene expression in cultured microglia derived from postmortem human brains
Auteurs : Max H. Walker [Canada] ; S. U. Kim [Canada] ; P. L. Mcgeer [Canada]Source :
- Journal of Neuroscience Research [ 0360-4012 ] ; 1995-03-01.
English descriptors
Abstract
Microglia were successfully cultured from human brain tissue from normal and neurologically diseased cases obtained 3.5–10 hours postmortem. Final cell preparations were more than 99% pure as judged by latex bead phagocytosis, expression of microglial phenotypic markers, and absence of astrocytic markers. The expression of complement genes C1qB, C3, and C4 as well as genes for interleukin‐(IL‐)1α, IL‐1β, IL‐6, tumor necrosis factor (TNF)α, IL‐1 receptor antagonist, and transforming growth factor β, but not inducible nitric oxide synthase, by these cells was detected by polymerase chain reaction (PCR) analysis. The pattern of gene expression was evaluated following stimulation of the cells with lipopolysaccharide, phorbol myristate acetate, γ interferon, and β amyloid peptide. There was considerable variation in gene response to these activating agents. However, it was of interest that β‐amyloid peptide (1–40) increased the expression of IL‐1β mRNA in these cells. The number of cases in this study was too small to permit evaluation of microglial response according to the disease state, but the results demonstrate the potential for such studies in the future. © 1995 Wiley‐Liss, Inc.
Url:
DOI: 10.1002/jnr.490400407
Affiliations:
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Walker</name><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>Kinsmen Laboratory of Neurological Research, Department of Psychiatry University of British Columbia, Vancouver, British Columbia</wicri:regionArea><wicri:noRegion>British Columbia</wicri:noRegion></affiliation><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>Kinsmen Laboratory of Neurological Research, Department of Psychiatry, 2255 Wesbrook Mall, Vancouver, B.C. V6T1Z3</wicri:regionArea><wicri:noRegion>B.C. V6T1Z3</wicri:noRegion></affiliation></author><author><name sortKey="Kim, S U" sort="Kim, S U" uniqKey="Kim S" first="S. U." last="Kim">S. U. 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Final cell preparations were more than 99% pure as judged by latex bead phagocytosis, expression of microglial phenotypic markers, and absence of astrocytic markers. The expression of complement genes C1qB, C3, and C4 as well as genes for interleukin‐(IL‐)1α, IL‐1β, IL‐6, tumor necrosis factor (TNF)α, IL‐1 receptor antagonist, and transforming growth factor β, but not inducible nitric oxide synthase, by these cells was detected by polymerase chain reaction (PCR) analysis. The pattern of gene expression was evaluated following stimulation of the cells with lipopolysaccharide, phorbol myristate acetate, γ interferon, and β amyloid peptide. There was considerable variation in gene response to these activating agents. However, it was of interest that β‐amyloid peptide (1–40) increased the expression of IL‐1β mRNA in these cells. The number of cases in this study was too small to permit evaluation of microglial response according to the disease state, but the results demonstrate the potential for such studies in the future. © 1995 Wiley‐Liss, Inc.</div></front></TEI><affiliations><list><country><li>Canada</li></country></list><tree><country name="Canada"><noRegion><name sortKey="Walker, Max H" sort="Walker, Max H" uniqKey="Walker M" first="Max H." last="Walker">Max H. Walker</name></noRegion><name sortKey="Kim, S U" sort="Kim, S U" uniqKey="Kim S" first="S. U." last="Kim">S. U. Kim</name><name sortKey="Mcgeer, P L" sort="Mcgeer, P L" uniqKey="Mcgeer P" first="P. L." last="Mcgeer">P. L. Mcgeer</name><name sortKey="Walker, Max H" sort="Walker, Max H" uniqKey="Walker M" first="Max H." last="Walker">Max H. Walker</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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