IRIS publication 120082729
Exposure of foetal neural progenitor cells to IL-1β impairs their proliferation and alters their differentiation - a role for maternal inflammation?
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TY - JOUR - Crampton S.J., Collins L.M., Toulouse A., Nolan Y.M., O'Keeffe G.W. - 2012 - Unknown - Journal of Neurochemistry - Exposure of foetal neural progenitor cells to IL-1β impairs their proliferation and alters their differentiation - a role for maternal inflammation? - Published - Altmetric: 1 () - 120 - 6 - 964 - 973 - 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. - 10.1111/j.1471-4159.2011.07634.x DA - 2012/NaN ER -
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@article{V120082729, = {Crampton S.J., Collins L.M. and Toulouse A., Nolan Y.M. and O'Keeffe G.W. }, = {2012}, = {Unknown}, = {Journal of Neurochemistry}, = {Exposure of foetal neural progenitor cells to IL-1β impairs their proliferation and alters their differentiation - a role for maternal inflammation?}, = {Published}, = {Altmetric: 1 ()}, = {120}, = {6}, pages = {964--973}, = {{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. }}, = {10.1111/j.1471-4159.2011.07634.x}, source = {IRIS} }
Data as stored in IRIS
AUTHORS | Crampton S.J., Collins L.M., Toulouse A., Nolan Y.M., O'Keeffe G.W. | ||
YEAR | 2012 | ||
MONTH | Unknown | ||
JOURNAL_CODE | Journal of Neurochemistry | ||
TITLE | Exposure of foetal neural progenitor cells to IL-1β impairs their proliferation and alters their differentiation - a role for maternal inflammation? | ||
STATUS | Published | ||
TIMES_CITED | Altmetric: 1 () | ||
SEARCH_KEYWORD | |||
VOLUME | 120 | ||
ISSUE | 6 | ||
START_PAGE | 964 | ||
END_PAGE | 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. | ||
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DOI_LINK | 10.1111/j.1471-4159.2011.07634.x | ||
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