Impact of prenatal arsenate exposure on gene expression in a pure population of migratory cranial neural crest cells.
作者： Partha Mukhopadhyay , Ratnam S. Seelan , Robert M. Greene , M. Michele Pisano
DOI: 10.1016/J.REPROTOX.2019.04.001
关键词:
摘要: Abstract Prenatal exposure to arsenic, a naturally occurring toxic element, causes neural tube defects (NTDs) and, in animal models, orofacial anomalies. Since aberrant development or migration of cranial crest cells (CNCCs) can also cause similar anomalies within developing embryos, we examined the effects utero sodium arsenate on gene expression patterns pure populations CNCCs, isolated by fluorescence activated cell sorting (FACS), from Cre/LoxP reporter mice. Changes were analyzed using Affymetrix GeneChip® microarrays and selected genes was verified TaqMan quantitative real-time PCR. We report, for first time, arsenate-induced alterations number novel candidate canonical cascades that may contribute pathogenesis defects. Ingenuity Pathway NIH-DAVID analyses revealed cellular response pathways, biological themes, potential upstream regulators, underlie altered fetal programming exposed CNCCs.
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