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Article: Transcriptomic and methylomic analysis reveal the toxicological effect of 2,3,7,8-Tetrachlorodibenzodioxin on human embryonic stem cell.

TitleTranscriptomic and methylomic analysis reveal the toxicological effect of 2,3,7,8-Tetrachlorodibenzodioxin on human embryonic stem cell.
Authors
Issue Date2018
PublisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/chemosphere
Citation
Chemosphere, 2018, v. 206, p. 663-673 How to Cite?
AbstractCumulating epidemiological studies demonstrated that environmental exposure to endocrine disrupting chemicals (EDCs) during the early stages of fetal development is associated with the increase in disease susceptibility in later life. The fetal developmental plasticity is considered as a protective mechanism against an undesirable prenatal environment. Dioxin is one of the environmental contaminants and is considered a diabetogenic factor. Experimental animal and human epidemiological studies have revealed that dioxin exposure was associated with insulin resistance and altered beta cell function. But the effect of dioxin exposure in early stage of fetal development is still largely unknown. In this report, we used the human embryonic stem cell (hESC) line, VAL-3, as a model, together with Methyl-CpG Binding Domain (MBD) protein-enriched genome sequencing and transcriptome sequencing (RNA-seq), in order to determine the dynamic changes of the epigenetic landscape and transcriptional dysregulation in hESC upon dioxin exposure. The bioinformatics analyses including the Database for Annotation, Visualization and Integrated Discovery (DAVID) analysis and Ingenuity Pathway Analysis (IPA) highlighted the predisposed neural, hepatic, cardiac and metabolic toxicological effects of dioxin during the fetal development.
Persistent Identifierhttp://hdl.handle.net/10722/263485
ISSN
2017 Impact Factor: 4.427
2015 SCImago Journal Rankings: 1.536
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLai, KP-
dc.contributor.authorLi, JW-
dc.contributor.authorChan, TF-
dc.contributor.authorChen, CH-
dc.contributor.authorLee, CYL-
dc.contributor.authorYeung, WSB-
dc.contributor.authorWong, CK-
dc.date.accessioned2018-10-22T07:39:43Z-
dc.date.available2018-10-22T07:39:43Z-
dc.date.issued2018-
dc.identifier.citationChemosphere, 2018, v. 206, p. 663-673-
dc.identifier.issn0045-6535-
dc.identifier.urihttp://hdl.handle.net/10722/263485-
dc.description.abstractCumulating epidemiological studies demonstrated that environmental exposure to endocrine disrupting chemicals (EDCs) during the early stages of fetal development is associated with the increase in disease susceptibility in later life. The fetal developmental plasticity is considered as a protective mechanism against an undesirable prenatal environment. Dioxin is one of the environmental contaminants and is considered a diabetogenic factor. Experimental animal and human epidemiological studies have revealed that dioxin exposure was associated with insulin resistance and altered beta cell function. But the effect of dioxin exposure in early stage of fetal development is still largely unknown. In this report, we used the human embryonic stem cell (hESC) line, VAL-3, as a model, together with Methyl-CpG Binding Domain (MBD) protein-enriched genome sequencing and transcriptome sequencing (RNA-seq), in order to determine the dynamic changes of the epigenetic landscape and transcriptional dysregulation in hESC upon dioxin exposure. The bioinformatics analyses including the Database for Annotation, Visualization and Integrated Discovery (DAVID) analysis and Ingenuity Pathway Analysis (IPA) highlighted the predisposed neural, hepatic, cardiac and metabolic toxicological effects of dioxin during the fetal development.-
dc.languageeng-
dc.publisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/chemosphere-
dc.relation.ispartofChemosphere-
dc.titleTranscriptomic and methylomic analysis reveal the toxicological effect of 2,3,7,8-Tetrachlorodibenzodioxin on human embryonic stem cell.-
dc.typeArticle-
dc.identifier.emailChen, CH: andycch0@hku.hk-
dc.identifier.emailLee, CYL: cherielee@hku.hk-
dc.identifier.emailYeung, WSB: wsbyeung@hku.hk-
dc.identifier.authorityLee, CYL=rp00308-
dc.identifier.authorityYeung, WSB=rp00331-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.chemosphere.2018.05.058-
dc.identifier.hkuros295250-
dc.identifier.volume206-
dc.identifier.spage663-
dc.identifier.epage673-
dc.identifier.isiWOS:000436215600074-
dc.publisher.placeUnited Kingdom-

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