Effect of Interleukin‐1β on the Expression of Actin Isoforms in Cultured Mouse Astroglia

Abstract

Cytokines are soluble mediators that are thought to act as communication signals between astroglia and neighboring neural cells. They are both released by, and act on, astroglia. It is hypothesized that it is this effect on astroglia that may be important in widespread phenomena including traumatic brain injury, inflammation, and scar formation. In this article, we examine the effect of mouse recombinant interleukin-1β (IL-1β) on the morphology, organization, and expression of glial fibrillary acidic protein (GFAP) and actin isoforms in cultured mouse astroglia. This study shows that the majority of the astroglia treated with IL-1β acquire long processes. Immunofluorescence staining shows that there are no remarkable changes in the organization of GFAP, F-actin, α-smooth muscle (α-sm) actin, and β-actin isoforms. In fluorescent microplate assay, the short-term treated astroglia (range, 1-2 days) show an increase in the intensity of GFAP and β-actin isoform over the level observed in untreated control, whereas no remarkable changes are observed in the intensity of α-sm actin isoform. In the case of long-term treatment (range, 4-8 days), the intensity of GFAP and α-sm actin isoform progressively decreases below the level of untreated control. In addition, the intensity of β-actin isoform increases above the control level. These results have been confirmed by immunoblotting experiments. The upregulation of β-actin isoform may be important in limiting the noxious effects of an inflammatory reaction. This gives credence to the hypothesis that it might be possible to modulate astroglial effects on neuronal inflammation and scar formation with appropriate therapies.