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      A novel regulatory network among LncRpa, CircRar1, MiR- 671 and apoptotic genes promotes lead-induced neuronal cell apoptosis

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          Abstract

          Lead is a metal that has toxic effects on the developing nervous system. However, the mechanisms underlying lead-induced neurotoxicity are not well understood. Non-coding RNAs (ncRNAs) play an important role in epigenetic regulation, but few studies have examined the function of ncRNAs in lead-induced neurotoxicity. We addressed this in the present study by evaluating the functions of a long non-coding RNA (named lncRpa) and a circular RNA (named circRar1) in a mouse model of lead-induced neurotoxicity. High-throughput RNA sequencing showed that both lncRpa and circRar1 promoted neuronal apoptosis. We also found that lncRpa and circRar1 induced the upregulation of apoptosis-associated factors caspase8 and p38 at the mRNA and protein levels via modulation of their common target microRNA miR- 671. This is the first report of a regulatory interaction among a lncRNA, circRNA, and miRNA mediating neuronal apoptosis in response to lead toxicity.

          Electronic supplementary material

          The online version of this article (doi:10.1007/s00204-016-1837-1) contains supplementary material, which is available to authorized users.

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          Long noncoding RNA as modular scaffold of histone modification complexes.

          Miao-Chih Tsai, Ohad Manor, Yue Wan … (2010)
          Long intergenic noncoding RNAs (lincRNAs) regulate chromatin states and epigenetic inheritance. Here, we show that the lincRNA HOTAIR serves as a scaffold for at least two distinct histone modification complexes. A 5' domain of HOTAIR binds polycomb repressive complex 2 (PRC2), whereas a 3' domain of HOTAIR binds the LSD1/CoREST/REST complex. The ability to tether two distinct complexes enables RNA-mediated assembly of PRC2 and LSD1 and coordinates targeting of PRC2 and LSD1 to chromatin for coupled histone H3 lysine 27 methylation and lysine 4 demethylation. Our results suggest that lincRNAs may serve as scaffolds by providing binding surfaces to assemble select histone modification enzymes, thereby specifying the pattern of histone modifications on target genes.
          Article 0 comments Cited 1275 times – based on 0 reviews     Review now
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            A coding-independent function of gene and pseudogene mRNAs regulates tumour biology

            Laura Poliseno, Leonardo Salmena, JiangWen Zhang … (2010)
            The canonical role of messenger RNA (mRNA) is to deliver protein-coding information to sites of protein synthesis. However, given that microRNAs bind to RNAs, we hypothesized that RNAs possess a biological role in cancer cells that relies upon their ability to compete for microRNA binding and is independent of their protein-coding function. As a paradigm for the protein-coding-independent role of RNAs, we describe the functional relationship between the mRNAs produced by the PTEN tumour suppressor gene and its pseudogene (PTENP1) and the critical consequences of this interaction. We find that PTENP1 is biologically active as determined by its ability to regulate cellular levels of PTEN, and that it can exert a growth-suppressive role. We also show that PTENP1 locus is selectively lost in human cancer. We extend our analysis to other cancer-related genes that possess pseudogenes, such as oncogenic KRAS. Further, we demonstrate that the transcripts of protein coding genes such as PTEN are also biologically active. Together, these findings attribute a novel biological role to expressed pseudogenes, as they can regulate coding gene expression, and reveal a non-coding function for mRNAs.
            Article 0 comments Cited 978 times – based on 0 reviews     Review now
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              Analysis of the mouse transcriptome based on functional annotation of 60,770 full-length cDNAs.

              Y Takenaka, Rodrigo Nakamura, C Bult … (2002)
              Only a small proportion of the mouse genome is transcribed into mature messenger RNA transcripts. There is an international collaborative effort to identify all full-length mRNA transcripts from the mouse, and to ensure that each is represented in a physical collection of clones. Here we report the manual annotation of 60,770 full-length mouse complementary DNA sequences. These are clustered into 33,409 'transcriptional units', contributing 90.1% of a newly established mouse transcriptome database. Of these transcriptional units, 4,258 are new protein-coding and 11,665 are new non-coding messages, indicating that non-coding RNA is a major component of the transcriptome. 41% of all transcriptional units showed evidence of alternative splicing. In protein-coding transcripts, 79% of splice variations altered the protein product. Whole-transcriptome analyses resulted in the identification of 2,431 sense-antisense pairs. The present work, completely supported by physical clones, provides the most comprehensive survey of a mammalian transcriptome so far, and is a valuable resource for functional genomics.
              Article 0 comments Cited 499 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Yiguo Jiang: +86 20 37103535 , jiangyiguo@vip.163.com
                Journal
                Journal ID (nlm-ta): Arch Toxicol
                Journal ID (iso-abbrev): Arch. Toxicol
                Title: Archives of Toxicology
                Publisher: Springer Berlin Heidelberg (Berlin/Heidelberg )
                ISSN (Print): 0340-5761
                ISSN (Electronic): 1432-0738
                Publication date (Electronic): 7 September 2016
                Publication date PMC-release: 7 September 2016
                Publication date (Print): 2017
                Volume: 91
                Issue: 4
                Pages: 1671-1684
                Affiliations
                [1 ]ISNI 0000 0000 8653 1072, GRID grid.410737.6, State Key Laboratory of Respiratory Disease, Institute for Chemical Carcinogenesis, , Guangzhou Medical University, ; Xinzao, Panyu District, Guangzhou, 511436 China
                [2 ]ISNI 0000 0001 2150 1785, GRID grid.17088.36, Department of Physiology, , Michigan State University, ; East Lansing, MI 48824 USA
                [3 ]ISNI 0000 0001 2150 1785, GRID grid.17088.36, Institute for Integrative Toxicology, , Michigan State University, ; East Lansing, MI 48824 USA
                Article
                Publisher ID: 1837
                DOI: 10.1007/s00204-016-1837-1
                PMC ID: 5364257
                PubMed ID: 27604105
                SO-VID: e328f3cf-e013-4bcc-a282-f1a5ed8eb968
                Copyright © © The Author(s) 2016
                License:

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

                History
                Date received : 27 May 2016
                Date accepted : 24 August 2016
                Funding
                Funded by: National Key Basic Research Program of China
                Award ID: 2012CB525004
                Award Recipient :
                Funded by: FundRef http://dx.doi.org/10.13039/501100001809, National Natural Science Foundation of China;
                Award ID: 21277036, 81573180, and 81172633
                Award Recipient :
                Funded by: Key Program of Guangdong Natural Science Foundation
                Award ID: 2014A030311017
                Award Recipient :
                Funded by: University Major Program of Guangdong
                Award ID: 2014SZD48
                Award Recipient :
                Funded by: University Talent Program of Guangdong
                Award ID: 2013-164
                Award Recipient :
                Funded by: University Chief Scientist Program of Guangzhou
                Award ID: 1201541575
                Award Recipient :
                Categories
                Subject: Toxicogenomics
                Custom metadata
                issue-copyright-statement © Springer-Verlag Berlin Heidelberg 2017

                ScienceOpen disciplines: Toxicology
                Keywords: circrna,lncrna,mirna,cell apoptosis,lead,neurotoxicity
                Data availability:
                ScienceOpen disciplines: Toxicology
                Keywords: circrna, lncrna, mirna, cell apoptosis, lead, neurotoxicity

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