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. 1992;84(4):387-93.
doi: 10.1007/BF00227665.

Immunohistochemical observations on rat radial glia: relationship with the origin of ethylnitrosourea-induced tumors

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Immunohistochemical observations on rat radial glia: relationship with the origin of ethylnitrosourea-induced tumors

M T Giordana et al. Acta Neuropathol. 1992.

Abstract

Gliomas induced in the rat by transplacental administration of ethylnitrosourea (ENU) are intensely immunoreactive for vimentin and scarcely for glial fibrillary acidic protein (GFAP). Since tumoral transformation takes place during the late fetal and early postnatal period, the sequential expression of the two glial antigens has been investigated in this age period in ENU-treated and control rats. Immunohistochemical and immunoelectron microscopical methods have been employed. Vimentin was widely expressed starting from embryonal day 14 (E 14) in the processes of radial glia; as long as radial glia was present, vimentin decorated it. GFAP was, at earliest, observed at E 20 and expressed by glial cells with a stellate, i.e., mature shape. No GFAP-positive radial process was observed. No difference was found between ENU-treated and control rats. Since ENU is most effective in producing tumors when administered at the 16-17th day of fetal life, vimentin-positive radial glia is a candidate target of ENU. The similarity of intermediate filament pattern between radial glia in the late fetal life and tumors induced by transplacental ENU suggests that radial glia might be the cell of origin.

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References

    1. J Neurol Sci. 1983 Oct-Nov;61(3):349-55 - PubMed
    1. Brain Res. 1983 Sep;285(3):317-36 - PubMed
    1. Acta Neuropathol. 1989;78(3):270-82 - PubMed
    1. Acta Neuropathol. 1986;70(3-4):209-19 - PubMed
    1. J Comp Neurol. 1976 Oct 1;169(3):291-312 - PubMed

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