ArticleBirth defects research. Part A, Clinical and molecular teratology2016
Effects of thyroxine exposure on the Twist 1 +/- phenotype: A test of gene-environment interaction modeling for craniosynostosis.
Article in Birth defects research. Part A, Clinical and molecular teratology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Article
- Manzamine-A AltersJournal of natural products · 2024Article
- Sfrp4 expression in thyroxine treated calvarial cells.Life sciences · 2022Article
- Pharmacological exposures may precipitate craniosynostosis through targeted stem cell depletion.Stem cell research · 2019Article
- Direct Effects of Nicotine Exposure on Murine Calvaria and Calvarial Cells.Scientific reports · 2019Article
- Selective serotonin re-uptake inhibitor sertraline inhibits bone healing in a calvarial defect model.International journal of oral science · 2018Article
- Gene/environment interactions in craniosynostosis: A brief review.Orthodontics & craniofacial research · 2017Review
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Authors and funding
9 authors.
Funding
Abstract
backgroundCraniosynostosis, the premature fusion of one or more of the cranial sutures, is estimated to occur in 1:1800 to 2500 births. Genetic murine models of craniosynostosis exist, but often imperfectly model human patients. Case, cohort, and surveillance studies have identified excess thyroid hormone as an agent that can either cause or exacerbate human cases of craniosynostosis.
methodsHere we investigate the influence of in utero and in vitro exogenous thyroid hormone exposure on a murine model of craniosynostosis, Twist 1 +/-.
resultsBy 15 days post-natal, there was evidence of coronal suture fusion in the Twist 1 +/- model, regardless of exposure. With the exception of craniofacial width, there were no significant effects of exposure; however, the Twist 1 +/- phenotype was significantly different from the wild-type control. Twist 1 +/- cranial suture cells did not respond to thyroxine treatment as measured by proliferation, osteogenic differentiation, and gene expression of osteogenic markers. However, treatment of these cells did result in modulation of thyroid associated gene expression.
conclusionOur findings suggest the phenotypic effects of the genetic mutation largely outweighed the effects of thyroxine exposure in the Twist 1 +/- model. These results highlight difficultly in experimentally modeling gene-environment interactions for craniosynostotic phenotypes. Birth Defects Research (Part A) 106:803-813, 2016. © 2016 Wiley Periodicals, Inc.
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