Retinoic Acid Drives Aryl Hydrocarbon Receptor Expression and Is Instrumental to Dioxin-Induced Toxicity during Palate Development
Author(s) -
Hugues Jacobs,
Christine Dennefeld,
Betty Féret,
Matti Viluksela,
Helen Håkansson,
Manuel Mark,
Norbert B. Ghyselinck
Publication year - 2011
Publication title -
environmental health perspectives
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.257
H-Index - 282
eISSN - 1552-9924
pISSN - 0091-6765
DOI - 10.1289/ehp.1003075
Subject(s) - aryl hydrocarbon receptor , retinoic acid , developmental toxicity , toxicity , teratology , mesenchyme , receptor , tretinoin , signal transduction , secondary palate , biology , retinoid , transgene , microbiology and biotechnology , chemistry , endocrinology , medicine , fetus , biochemistry , embryo , cell culture , genetics , transcription factor , anatomy , gene , pregnancy
Palate development depends on complex events and is very sensitive to disruption. Accordingly, clefts are the most common congenital malformations worldwide, and a connection is proposed with fetal exposure to toxic factors or environmental contaminants, such as dioxins. There is increasing evidence that dioxin interferes with all-trans-retinoic acid (atRA), a hormone-like signal derived from vitamin A, which plays an essential role during embryonic development. Although similarities have been described between dioxin-induced toxicity and the outcome of altered atRA signaling during palate development, their relationship needs to be clarified.
Accelerating Research
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom
Address
John Eccles HouseRobert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom