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      Corrigendum to “miR-1-Mediated Induction of Cardiogenesis in Mesenchymal Stem Cells via Downregulation of Hes-1”

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          Abstract

          In Figure 2(a) of the published article entitled “miR-1-Mediated Induction of Cardiogenesis in Mesenchymal Stem Cells via Downregulation of Hes-1,” [1] the authors admit to being careless in altering nonspecific belts, stains, or scratches in the Nkx2.5, cTnT, and CX43 panels. The original figures are presented here.

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          miR-1-Mediated Induction of Cardiogenesis in Mesenchymal Stem Cells via Downregulation of Hes-1

          Yun-Feng Huang, Liang Tang, Zhen-fei Fang … (2012)
          MicroRNAs (miRNAs, miRs) have the potential to control stem cells fate decisions. The cardiac- and skeletal-muscle-specific miRNA, miR-1, can regulate embryonic stem cells differentiation to cardiac lineage by suppressing gene expression of alternative lineages. Accordingly, we hypothesized that overexpression of miR-1 may also promote cardiac gene expression in mesenchymal stem cells. Since Notch signaling could inhibit muscle differentiation, a process in contrast with the effect of miR-1, miR-1-mediated repression of Notch signaling may contribute to the observed effects of miR-1 in mesenchymal stem cells. Thus, mesenchymal stem cells were infected by lentiviral vectors carrying miR-1, and cells expressing miR-1 were selected. Alterations in Notch signaling and cardiomyocyte markers, Nkx2.5, GATA-4, cTnT, and CX43, were identified by Western blot in the infected cells on days 1, 7, and 14. Our study showed that the downstream target molecule of Notch pathway, Hes-1, was obviously decreased in mesenchymal stem cells modified with miR-1, and overexpression of miR-1 promotes the specific cardiac gene expression in the infected cells. Knockdown of Hes-1 leads to the same effects on cell lineage decisions. Our results indicated that miR-1 promotes the differentiation of MSCs into cardiac lineage in part due to negative regulation of Hes-1.
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            Author and article information

            Journal
            Journal ID (nlm-ta): Biomed Res Int
            Journal ID (iso-abbrev): Biomed Res Int
            Journal ID (publisher-id): BMRI
            Title: BioMed Research International
            Publisher: Hindawi Publishing Corporation
            ISSN (Print): 2314-6133
            ISSN (Electronic): 2314-6141
            Publication date (Print): 2016
            Publication date (Electronic): 14 September 2016
            Volume: 2016
            Electronic Location Identifier: 8510747
            Affiliations
            Department of Cardiology, The Second Xiangya Hospital of Central South University, Hunan, Changsha 410011, China
            Author notes
            Author information
            http://orcid.org/0000-0002-0404-5260
            Article
            DOI: 10.1155/2016/8510747
            PMC ID: 5039301
            PubMed ID: 27703981
            SO-VID: 088d4650-50d3-43fc-8200-9726f576b654
            Copyright © Copyright © 2016 Feng Huang et al.
            License:

            This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

            History
            Date received : 7 December 2015
            Date accepted : 24 May 2016
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            Subject: Corrigendum

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