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Article: Enhanced Inflammatory Response in Neural Tubes of Embryos Derived from Diabetic Mice Exposed to a Teratogen

TitleEnhanced Inflammatory Response in Neural Tubes of Embryos Derived from Diabetic Mice Exposed to a Teratogen
Authors
Issue Date2004
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/34828
Citation
Journal Of Neuroscience Research, 2004, v. 75 n. 4, p. 554-564 How to Cite?
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-α (TNF-α) 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.
Persistent Identifierhttp://hdl.handle.net/10722/162754
ISSN
2015 Impact Factor: 2.689
2015 SCImago Journal Rankings: 1.261
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLian, Qen_US
dc.contributor.authorDheen, STen_US
dc.contributor.authorLiao, Den_US
dc.contributor.authorTay, SSWen_US
dc.date.accessioned2012-09-05T05:23:06Z-
dc.date.available2012-09-05T05:23:06Z-
dc.date.issued2004en_US
dc.identifier.citationJournal Of Neuroscience Research, 2004, v. 75 n. 4, p. 554-564en_US
dc.identifier.issn0360-4012en_US
dc.identifier.urihttp://hdl.handle.net/10722/162754-
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-α (TNF-α) 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.en_US
dc.languageengen_US
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/34828en_US
dc.relation.ispartofJournal of Neuroscience Researchen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCytokines - Metabolismen_US
dc.subject.meshDiabetes Mellitus, Experimental - Embryology - Metabolism - Pathologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshInflammation - Embryology - Metabolismen_US
dc.subject.meshMiceen_US
dc.subject.meshMicroglia - Drug Effects - Metabolism - Pathologyen_US
dc.subject.meshNervous System - Embryology - Metabolism - Pathologyen_US
dc.subject.meshPregnancyen_US
dc.subject.meshPrenatal Exposure Delayed Effectsen_US
dc.subject.meshTeratogens - Toxicityen_US
dc.titleEnhanced Inflammatory Response in Neural Tubes of Embryos Derived from Diabetic Mice Exposed to a Teratogenen_US
dc.typeArticleen_US
dc.identifier.emailLian, Q:qzlian@hkucc.hku.hken_US
dc.identifier.authorityLian, Q=rp00267en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1002/jnr.20006en_US
dc.identifier.pmid14743439-
dc.identifier.scopuseid_2-s2.0-0742322772en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0742322772&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume75en_US
dc.identifier.issue4en_US
dc.identifier.spage554en_US
dc.identifier.epage564en_US
dc.identifier.isiWOS:000188740900012-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridLian, Q=7003399023en_US
dc.identifier.scopusauthoridDheen, ST=6701666815en_US
dc.identifier.scopusauthoridLiao, D=7202026835en_US
dc.identifier.scopusauthoridTay, SSW=7102586515en_US

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