title: Maternal thyroid hormone increases HES expression in the fetal rat brain: an effect mimicked by exposure to a mixture of polychlorinated biphenyls (PCBs).
abstract: Thyroid hormone is known to be essential for normal brain development both before and after birth, but much less is known about the role of thyroid hormone development before birth. In rodents, thyroid hormone of maternal origin can selectively regulate gene expression in the fetal cortex; HES1 was identified as a putative thyroid hormone responsive gene in the fetal cortex. Using in situ hybridization, we now confirm that thyroid hormone administration to pregnant rats can increase the abundance of HES1 mRNA in the fetal cortex on gestational day 16 (G16). In separate experiments, we found that maternal exposure to polychlorinated biphenyls (PCBs) increases HES expression similarly. Western analysis of proteins extracted from fetal cortex did not confirm that Notch-1 or Notch-3 activation was associated with treatment effects on HES expression. However, considering the role of HES proteins in fate specification of cortical neurons, these findings suggest that thyroid hormone, and PCB exposure, may influence fate specification of cortical neurons.
authors.affiliation: Department of Biology, University of Massachusetts-Amherst, Morrill Science Center, Amherst, MA 01003, USA.
authors.forename: Ruby
authors.initials: R
authors.lastname: Bansal
authors.forename: Seo-Hee
authors.initials: SH
authors.lastname: You
authors.forename: Carolyn T A
authors.initials: CT
authors.lastname: Herzig
authors.forename: R Thomas
authors.initials: RT
authors.lastname: Zoeller
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001345:Autoradiography / Q000379:methods; D051792:Basic Helix-Loop-Helix Proteins; D015153:Blotting, Western / Q000379:methods; D002540:Cerebral Cortex / Q000187:drug effects* / Q000196:embryology / Q000378:metabolism; D004268:DNA-Binding Proteins / Q000235:genetics / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D004347:Drug Interactions; D004622:Embryo, Mammalian; D005260:Female; D015870:Gene Expression / Q000187:drug effects*; D018507:Gene Expression Regulation, Developmental / Q000187:drug effects; D018398:Homeodomain Proteins / Q000235:genetics / Q000378:metabolism*; D017403:In Situ Hybridization / Q000379:methods; D011078:Polychlorinated Biphenyls / Q000494:pharmacology*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D012333:RNA, Messenger / Q000378:metabolism; D011863:Radioimmunoassay / Q000379:methods; D051381:Rats; D017207:Rats, Sprague-Dawley; D012097:Repressor Proteins / Q000235:genetics / Q000378:metabolism; D013963:Thyroid Hormones / Q000097:blood / Q000494:pharmacology*; D000072056:Transcription Factor HES-1; D014404:Tubulin / Q000235:genetics / Q000378:metabolism
chemical_list: D051792:Basic Helix-Loop-Helix Proteins; D004268:DNA-Binding Proteins; D018398:Homeodomain Proteins; D011078:Polychlorinated Biphenyls; D012333:RNA, Messenger; D012097:Repressor Proteins; D013963:Thyroid Hormones; D000072056:Transcription Factor HES-1; D014404:Tubulin; C489735:Hes1 protein, rat; C489686:Hes5 protein, rat