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- W2037795854 abstract "Abstract Peroxisome proliferator‐activated receptor gamma (PPAR‐γ) is a member of the nuclear hormone superfamily originally characterized as a regulator of adipocyte differentiation and lipid metabolism. In addition, PPAR‐γ has important immunomodulatory functions. If the effect of PPAR‐γ's activation in T‐cell‐mediated demyelination has been recently demonstrated, nothing is known about the role of PPAR‐γ in antibody‐induced demyelination in the absence of T‐cell interactions and monocyte/macrophage activation. Therefore, we investigated PPAR‐γ's involvement by using an in vitro model of inflammatory demyelination in three‐dimensional aggregating rat brain cell cultures. We found that PPAR‐γ was not constitutively expressed in these cultures but was strongly up‐regulated following demyelination mediated by antibodies directed against myelin oligodendrocyte glycoprotein (MOG) in the presence of complement. Pioglitazone, a selective PPAR‐γ agonist, partially protected aggregates from anti‐MOG demyelination. Heat shock responses and the expression of the proinflammatory cytokine tumor necrosis factor‐α were diminished by pioglitazone treatment. Therefore, pioglitazone protection seems to be linked to an inhibition of glial cell proinflammatory activities following anti‐MOG induced demyelination. We show that PPAR‐γ agonists act not only on T cells but also on antibody‐mediated demyelination. This may represent a significant benefit in treating multiple sclerosis patients. © 2002 Wiley‐Liss, Inc." @default.
- W2037795854 created "2016-06-24" @default.
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- W2037795854 date "2002-12-24" @default.
- W2037795854 modified "2023-10-15" @default.
- W2037795854 title "Inhibition of glial cell proinflammatory activities by peroxisome proliferator-activated receptor gamma agonist confers partial protection during antimyelin oligodendrocyte glycoprotein demyelination in vitro" @default.
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- W2037795854 doi "https://doi.org/10.1002/jnr.10471" @default.
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