UM  > Faculty of Health Sciences
Residential Collegefalse
Status已發表Published
Methylmercury exposure increases lipocalin related (lpr) and decreases activated in blocked unfolded protein response (abu) genes and specific mirnas in caenorhabditis elegans
Rudgalvyte M.1; VanDuyn N.2; Aarnio V.1; Heikkinen L.1; Peltonen J.1; Lakso M.1; Nass R.2; Wong G.1
2013-10-04
Source PublicationToxicology Letters
ISSN03784274 18793169
Volume222Issue:2Pages:189-196
Abstract

Methylmercury (MeHg) is a persistent environmental and dietary contaminant that causes serious adverse developmental and physiologic effects at multiple cellular levels. In order to understand more fully the consequences of MeHg exposure at the molecular level, we profiled gene and miRNA transcripts from the model organism Caenorhabditis elegans. Animals were exposed to MeHg (10. μM) from embryo to larval 4 (L4) stage and RNAs were isolated. RNA-seq analysis on the Illumina platform revealed 541 genes up- and 261 genes down-regulated at a cutoff of 2-fold change and false discovery rate-corrected significance q<0.05. Among the up-regulated genes were those previously shown to increase under oxidative stress conditions including hsp-16.11 (2.5-fold), gst-35 (10.1-fold), and fmo-2 (58.5-fold). In addition, we observed up-regulation of 6 out of 7 lipocalin related (lpr) family genes and down regulation of 7 out of 15 activated in blocked unfolded protein response (abu) genes. Gene Ontology enrichment analysis highlighted the effect of genes related to development and organism growth. miRNA-seq analysis revealed 6-8 fold down regulation of mir-37-3p, mir-41-5p, mir-70-3p, and mir-75-3p. Our results demonstrate the effects of MeHg on specific transcripts encoding proteins in oxidative stress responses and in ER stress pathways. Pending confirmation of these transcript changes at protein levels, their association and dissociation characteristics with interaction partners, and integration of these signals, these findings indicate broad and dynamic mechanisms by which MeHg exerts its harmful effects. © 2013 The Authors.

KeywordBlocked Unfolded Protein Response Er Stress Heavy Metal Next-generation Sequencing Oxidative Stress
DOI10.1016/j.toxlet.2013.07.014
URLView the original
Indexed BySCIE
Language英語English
WOS Research AreaToxicology
WOS SubjectToxicology
WOS IDWOS:000324301900012
Scopus ID2-s2.0-84882746365
Fulltext Access
Citation statistics
Document TypeJournal article
CollectionFaculty of Health Sciences
Affiliation1.Itä-Suomen yliopisto
2.Indiana University School of Medicine Indianapolis
Recommended Citation
GB/T 7714
Rudgalvyte M.,VanDuyn N.,Aarnio V.,et al. Methylmercury exposure increases lipocalin related (lpr) and decreases activated in blocked unfolded protein response (abu) genes and specific mirnas in caenorhabditis elegans[J]. Toxicology Letters, 2013, 222(2), 189-196.
APA Rudgalvyte M.., VanDuyn N.., Aarnio V.., Heikkinen L.., Peltonen J.., Lakso M.., Nass R.., & Wong G. (2013). Methylmercury exposure increases lipocalin related (lpr) and decreases activated in blocked unfolded protein response (abu) genes and specific mirnas in caenorhabditis elegans. Toxicology Letters, 222(2), 189-196.
MLA Rudgalvyte M.,et al."Methylmercury exposure increases lipocalin related (lpr) and decreases activated in blocked unfolded protein response (abu) genes and specific mirnas in caenorhabditis elegans".Toxicology Letters 222.2(2013):189-196.
Files in This Item:
There are no files associated with this item.
Related Services
Recommend this item
Bookmark
Usage statistics
Export to Endnote
Google Scholar
Similar articles in Google Scholar
[Rudgalvyte M.]'s Articles
[VanDuyn N.]'s Articles
[Aarnio V.]'s Articles
Baidu academic
Similar articles in Baidu academic
[Rudgalvyte M.]'s Articles
[VanDuyn N.]'s Articles
[Aarnio V.]'s Articles
Bing Scholar
Similar articles in Bing Scholar
[Rudgalvyte M.]'s Articles
[VanDuyn N.]'s Articles
[Aarnio V.]'s Articles
Terms of Use
No data!
Social Bookmark/Share
All comments (0)
No comment.
 

Items in the repository are protected by copyright, with all rights reserved, unless otherwise indicated.