Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/44600
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dc.contributor.authorTonack, S.en
dc.contributor.authorKind, K.en
dc.contributor.authorThompson, J.en
dc.contributor.authorWobus, A.en
dc.contributor.authorFischer, B.en
dc.contributor.authorSantos, A.en
dc.date.issued2007en
dc.identifier.citationEndocrinology, 2007; 148(12):5902-5912en
dc.identifier.issn0013-7227en
dc.identifier.issn0013-7227en
dc.identifier.urihttp://hdl.handle.net/2440/44600-
dc.descriptionCopyright © 2007 by The Endocrine Societyen
dc.description.abstractIntoxication by dioxins such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) leads, among other damages, to early embryo loss, fetal malformations, and cardiovascular toxicity. Apart from binding to the arylhydrocarbon receptor (AhR), the mechanism of TCDD-mediated embryo toxicity is still unclear. We investigated possible modes of a TCDD-mediated toxicity, particularly in glucose metabolism, in pluripotent P19 mouse embryonic carcinoma cells. Undifferentiated P19 cells were exposed to 1–100 nM TCDD and characterized for AhR signaling. For studying cell differentiation, P19 cells were exposed to 10 nM TCDD at stage of embryoid body formation, and analyzed on glucose metabolism and cardiac differentiation during the next 3 wk. TCDD treatment activated the AhR-signaling cascade within 1 h, confirmed by AhR translocation, induction of cytochrome P450 1A1 expression, and activation of the xenobiotic response element. Although cell viability and transcription of the cardiac marker protein - αmyosin heavy chain were affected, TCDD did not inhibit the differentiation of P19 cells to pulsating cardiomyocytes. TCDD significantly down-regulated the expression levels of the glucose transporter (GLUT) isoforms 1 and 3. After 24-h TCDD treatment, GLUT1 was no longer localized in the plasma membrane of P19 cells. The impaired GLUT expression correlated with a lower glucose uptake in 5-d-old embryoid bodies. The TCDD effects were mediated by AhR, as shown by preculture with the AhR antagonist -αnaphthoflavone. Our data demonstrate that an AhR-mediated disturbance in GLUT expression and insufficient glucose uptake may be major mechanisms in TCDD embryo toxicity.en
dc.description.statementofresponsibilitySarah Tonack, Karen Kind, Jeremy G. Thompson, Anna M. Wobus, Bernd Fischer and Anne Navarrete Santosen
dc.language.isoenen
dc.publisherEndocrine Socen
dc.subjectglucose transporter isoforms; GLUT; TCDD; dioxin; embryonic carcinoma cells; P19-EC cells; myogenic development; cardiogenesis; alpha myosin heavy chain; MyoD; desmin; XRE; alpha naphtoflavone; AhR; CYP1A1en
dc.titleDioxin affects glucose transport via the arylhydrocarbon receptor signal cascade in pluripotent embryonic carcinoma cellsen
dc.typeJournal articleen
dc.identifier.rmid0020073592en
dc.identifier.doi10.1210/en.2007-0254en
dc.identifier.pubid46956-
pubs.library.collectionObstetrics and Gynaecology publicationsen
pubs.verification-statusVerifieden
pubs.publication-statusPublisheden
dc.identifier.orcidThompson, J. [0000-0003-4941-7731]en
Appears in Collections:Obstetrics and Gynaecology publications

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