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dc.contributor.authorGarland, Michael A
dc.contributor.authorSengupta, Sumitra
dc.contributor.authorMathew, Lijoy K
dc.contributor.authorTruong, Lisa
dc.contributor.authorde Jong, Esther
dc.contributor.authorPiersma, Aldert H
dc.contributor.authorLa Du, Jane
dc.contributor.authorTanguay, Robert L
dc.date.accessioned2019-10-04T09:32:28Z
dc.date.available2019-10-04T09:32:28Z
dc.date.issued2019-01-01
dc.identifier.issn2214-7500
dc.identifier.pmid31249786
dc.identifier.doi10.1016/j.toxrep.2019.05.013
dc.identifier.urihttp://hdl.handle.net/10029/623303
dc.description.abstractWe previously used a chemical genetics approach with the larval zebrafish to identify small molecule inhibitors of tissue regeneration. This led to the discovery that glucocorticoids (GC) block early stages of tissue regeneration by the inappropriate activation of the glucocorticoid receptor (GR). We performed a microarray analysis to identify the changes in gene expression associated with beclomethasone dipropionate (BDP) exposure during epimorphic fin regeneration. Oncofetal cripto-1 showed > eight-fold increased expression in BDP-treated regenerates. We hypothesized that the mis-expression of cripto-1 was essential for BDP to block regeneration. Expression of cripto-1 was not elevated in GR morphants in the presence of BDP indicating that cripto-1 induction was GR-dependent. Partial translational suppression of Cripto-1 in the presence of BDP restored tissue regeneration. Retinoic acid exposure prevented increased cripto-1 expression and permitted regeneration in the presence of BDP. We demonstrated that BDP exposure increased cripto-1 expression in mouse embryonic stem cells and that regulation of cripto-1 by GCs is conserved in mammals.en_US
dc.language.isoenen_US
dc.subjectAEC, apical epithelial capen_US
dc.subjectBDP, beclomethasone dipropionateen_US
dc.subjectBeclomethasone dipropionateen_US
dc.subjectCripto-1en_US
dc.subjectDMSO, dimethyl sulfoxideen_US
dc.subjectEB, embryoid bodyen_US
dc.subjectECM, extracellular matrixen_US
dc.subjectEMT, epithelial-to-mesenchymal transitionen_US
dc.subjectERK, extracellular signal-regulated kinaseen_US
dc.subjectEpimorphic regenerationen_US
dc.subjectFGF, fibroblast growth factoren_US
dc.subjectGC, glucocorticoiden_US
dc.subjectGR, glucocorticoid receptoren_US
dc.subjectGlucocorticoidsen_US
dc.subjectISH, in situ hybridizationen_US
dc.subjectMIAME, Minimum Information About a Microarray Experimenten_US
dc.subjectMO, morpholino oligonucleotideen_US
dc.subjectOne-eyed pinheaden_US
dc.subjectRA, retinoic aciden_US
dc.subjectSEM, standard error of the meanen_US
dc.subjectTGF-β, transforming growth factor betaen_US
dc.subjectZebrafishen_US
dc.subjectdpa, days post-amputationen_US
dc.subjectdpf, days post-fertilizationen_US
dc.subjecteSC, embryonic stem cellen_US
dc.subjecthpa, hours post-amputationen_US
dc.subjecthpf, hours post-fertilizationen_US
dc.subjectmLIF, murine leukemia inhibitory factoren_US
dc.subjectqRT-PCR, quantitative reverse transcription polymerase chain reactionen_US
dc.subjectzf, zebrafishen_US
dc.titleGlucocorticoid receptor-dependent induction of () inhibits zebrafish caudal fin regeneration.en_US
dc.typeArticleen_US
dc.identifier.journalToxicol Rep 2019; 6:529-537en_US
dc.source.journaltitleToxicology reports


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