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• W1657402881 abstract "J. Neurochem. (2012) 120, 964–973. Abstract During pregnancy, activation of the maternal immune system results in inflammation in the foetal nervous system. The causative agents are pro-inflammatory cytokines like interleukin-1β (IL-1β), produced by the foetus. In this study, we examine the effect of IL-1β on the proliferation and differentiation of neural progenitor cells (NPCs) to better understand its potential effects on the developing brain. We find that the IL-1β receptor (IL-1R1) is expressed in the ventral mesencephalon of the developing brain. Furthermore, IL-1R1 is expressed on Nestin-positive, Sox-2-positive NPCs. IL-1β treatment reduced the numbers of proliferating NPCs, an effect prevented by the IL-1R1 receptor antagonist. LDH and MTT assays, and western blot analysis for cleaved caspase 3 and poly(ADP-ribose) polymerase, confirmed that this was not due to an increase in cell death but rather an induction of differentiation. To further study the effects of IL-1β on cell fate determination, we differentiated NPCs in the presence and absence of IL-1β. Il-1β promoted gliogenesis and inhibited neurogenesis, an effect that required p38-MAPK kinase signalling. In summary, these data show that exposure of NPCs to IL-1β affects their development. This necessitates an examination of the consequences that maternal immune system activation during pregnancy has on the cellular architecture of the developing brain." @default.
• W1657402881 created "2016-06-24" @default.
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• W1657402881 date "2012-01-01" @default.
• W1657402881 modified "2023-09-27" @default.
• W1657402881 title "Exposure of foetal neural progenitor cells to IL-1β impairs their proliferation and alters their differentiation - a role for maternal inflammation?" @default.
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• W1657402881 doi "https://doi.org/10.1111/j.1471-4159.2011.07634.x" @default.
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