Please use this identifier to cite or link to this item: https://doi.org/10.1002/jnr.20006
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dc.titleEnhanced Inflammatory Response in Neural Tubes of Embryos Derived from Diabetic Mice Exposed to a Teratogen
dc.contributor.authorLian, Q.
dc.contributor.authorDheen, S.T.
dc.contributor.authorLiao, D.
dc.contributor.authorTay, S.S.W.
dc.date.accessioned2012-06-08T09:23:40Z
dc.date.available2012-06-08T09:23:40Z
dc.date.issued2004-02-15
dc.identifier.citationLian, Q., Dheen, S.T., Liao, D., Tay, S.S.W. (2004-02-15). Enhanced Inflammatory Response in Neural Tubes of Embryos Derived from Diabetic Mice Exposed to a Teratogen. Journal of Neuroscience Research 75 (4) : 554-564. ScholarBank@NUS Repository. https://doi.org/10.1002/jnr.20006
dc.identifier.issn0360-4012
dc.identifier.issn1097-4547
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/163923
dc.description.abstractExposure of embryos to the teratogen cyclophosphamide (CP) and maternal diabetes is linked to pathogenesis of neural tube defects during development. Maternal diabetes aggravates the teratogen-induced inflammatory reaction leading to increased risk of neural tube defects in mouse embryos. The inflammatory reaction in the developing neural tube has been characterized by the presence of activated amoeboid microglia/brain macrophages and altered expression levels of cytokines. Although there were no obvious anomalies observed in the neural tubes of embryos from CP-treated nondiabetic mice, the frequency of neural tube defects was increased significantly in embryos of CP-treated diabetic mice. Moreover, there were more activated amoeboid microglia in the forebrain of CP-treated diabetic embryos compared to that in CP-treated non-diabetic mice. The expression of cytokines such as tumor necrosis factor-β (TNF-β) and transforming growth factor-β1 (TGF-β1) in the fetal brain of normal and diabetic embryos was induced in the neural tubes after CP treatment. Furthermore, the mRNA expression levels of both genes were increased markedly in the neural tube of CP-treated diabetic embryos compared to that of CP-treated non-diabetic embryos as measured by quantitative real-time PCR. Immunohistochemically, more TNF-α- and TGF-β1-positive cells, which included neurons and amoeboid microglia, were detected in CP-treated diabetic embryos than in CP-treated normal embryos. Maternal diabetes aggravates teratogen-induced inflammation, which is characterized in the developing neural tube by increased amoeboid microglia and enhanced expression of inflammatory cytokines. Although a definite link has yet to be elucidated, it is suggested that the increased rate of neural tube defects observed in CP-treated diabetic embryos may be due to upregulation of proinflammatory cytokines caused by maternal diabetes. © 2004 Wiley-Liss, Inc.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1002/jnr.20006
dc.language.isoen
dc.publisherWiley
dc.sourceScopus
dc.subjectAmoeboid microglia/brain macrophage
dc.subjectCyclophosphamide
dc.subjectDiabetic embryos
dc.subjectTGF-β1, neural tube defects
dc.subjectTNF-α
dc.typeArticle
dc.date.updated2020-01-17T07:57:59Z
dc.contributor.departmentDEPT OF ANATOMY
dc.description.doi10.1002/jnr.20006
dc.description.sourcetitleJournal of Neuroscience Research
dc.description.volume75
dc.description.issue4
dc.description.page554-564
dc.description.codenJNRED
dc.identifier.isiut000188740900012
dc.description.placeUnited States
dc.published.statePublished
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