Transforming growth factor-beta 1 in the rat brain: increase after injury and inhibition of astrocyte proliferation.
作者： D Lindholm , E Castrén , R Kiefer , F Zafra , H Thoenen
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摘要: Transforming growth factor-beta 1 (TGF-beta 1) has been shown to up-regulate the synthesis of nerve factor (NGF) in cultured rat astrocytes and neonatal brain vivo (Lindholm, D., B. Hengerer, F. Zafra, H. Thoenen. 1990. NeuroReport. 1:9-12). Here we show that mRNA encoding TGF-beta increased cerebral cortex after a penetrating injury. The level NGF is also transiently trauma, whereas brain-derived neurotrophic remained unchanged. In situ hybridization experiments showed strong expression 4 d lesion cells within vicinity wound. Staining adjacent sections with OX-42 antibodies, specific for macrophages microglia/brain macrophages, revealed similar pattern positive cells, suggesting invading perhaps reactive microglia, are source injured brain. Both microglia express culture, levels by various factors, including FGF, EGF, itself. inhibitor astrocyte proliferation suppresses mitotic effects FGF EGF on astrocytes. present results indicate expressed lesioned plays role regeneration stimulating production controlling extent scar formation.
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