Glial cell effects proliferation

Activated macrophages and microglia are likely cellular sources of IL-1 in the central nervous system. IL-la and p, both 17-kDa proteins, are the products of two distinct genes and produce many of the same effects that TNF has on glial cells. IL-1 upregulates cytokine production, includes cell surface molecules, activates nitric oxide, and stimulates proliferation. When used alone, IL-1 and TNFa both stimulate nitric oxide production in C6 cells. However, in human fetal astrocyte cultures, IL-1 is a better nitric oxide inducer when used in combination with IFNy. 

Microglia-derived interleukins have been shown to have effects on microglia and other glial cell types. IL-1 is a pluripotent and multifunctional molecule that mediates lymphocyte activation, fibroblast proliferation, and endogenous pyrogen-esis.77 Following treatment with IL-1, cultured astrocytes proliferate, indicating that... 

Glial cells as well as neurons can respond to FGF-2. One of the most significant effects of FGF-2 is its induction of glial cell proliferation, documented in vitro with astroglia (Sensenbrenner et al., 1987) as well as with oligodendrocytes (Eccleston and Silberberg, 1985 Besnard et al.,... 

Scherer, J. and Schnitzer, J. (1994) Growth factor effects on the proliferation of different retinal glial cells in vitro. Dev. Brain Res. 80 209-221. 

In primary cultures from developing rat or mouse cerebellum no such effects on proliferation of EGL cells has been demonstrated (Messer et al. 1984, 1985), although effects on the number of glial cells were found. However, it is not clear whether proliferation of EGL cells occurs at sufficient levels in these cultures to show effects even if they were present. Thus, this issue must await further clarification. Also there is some question as to whether all postnatal germinal zones respond to thyroid hormones in the same way (Seress, 1977, 1978). However, the presence of specific nuclear receptors for thyroid hormones during brain development, (see Chapter by DeNayer) is consistent with the possibility that effects of thyroid hormones on cell proliferation, where they do exist, could occur by direct interactions with the genome. 

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