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      Correction: Role of MicroRNA 1207-5P and Its Host Gene, the Long Non-Coding RNA Pvt1, as Mediators of Extracellular Matrix Accumulation in the Kidney: Implications for Diabetic Nephropathy

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          Abstract

          The author list for this article is corrected to list Dr. Johanna K. DiStefano as the fifth author of the article. Johanna DiStefano’s inclusion as an author is in line with the recommendation of the Translational Genomics Research Institute, which evaluated the contributions to this work. The first and corresponding author M. Lucrecia Alvarez disagrees with the addition of Johanna K. DiStefano to the author list, as she considers that Dr. DiStefano did not contribute to this publication. Dr. Alvarez also states her disagreement to the additions to the Author Contributions listed below. The revised author list is: M. Lucrecia Alvarez, Mahdieh Khosroheidari, Elena Eddy, Jeff Kiefer, Johanna K. DiStefano The affiliation for Johanna DiStefano at the time of the study was: Diabetes, Cardiovascular and Metabolic Diseases Center, Translational Genomics Research Institute, Phoenix The revised Authors Contributions are: Conceived and designed the experiments: MLA JKD. Performed the experiments: MLA MK EE. Analyzed the data: MLA MK EE JK. Contributed reagents/materials/analysis tools: MLA. Wrote the paper: MLA JKD. The revised citation is: Alvarez ML, Khosroheidari M, Eddy E, Kiefer J, DiStefano JK (2013) Role of MicroRNA 1207-5P and Its Host Gene, the Long Non-Coding RNA Pvt1, as Mediators of Extracellular Matrix Accumulation in the Kidney: Implications for Diabetic Nephropathy. PLoS ONE 8(10): e77468. doi:10.1371/journal.pone.0077468

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          Role of MicroRNA 1207-5P and Its Host Gene, the Long Non-Coding RNA Pvt1, as Mediators of Extracellular Matrix Accumulation in the Kidney: Implications for Diabetic Nephropathy

          Diabetic nephropathy is the most common cause of chronic kidney failure and end-stage renal disease in the Western World. One of the major characteristics of this disease is the excessive accumulation of extracellular matrix (ECM) in the kidney glomeruli. While both environmental and genetic determinants are recognized for their role in the development of diabetic nephropathy, epigenetic factors, such as DNA methylation, long non-coding RNAs, and microRNAs, have also recently been found to underlie some of the biological mechanisms, including ECM accumulation, leading to the disease. We previously found that a long non-coding RNA, the plasmacytoma variant translocation 1 (PVT1), increases plasminogen activator inhibitor 1 (PAI-1) and transforming growth factor beta 1 (TGF-β1) in mesangial cells, the two main contributors to ECM accumulation in the glomeruli under hyperglycemic conditions, as well as fibronectin 1 (FN1), a major ECM component. Here, we report that miR-1207-5p, a PVT1-derived microRNA, is abundantly expressed in kidney cells, and is upregulated by glucose and TGF-β1. We also found that like PVT1, miR-1207-5p increases expression of TGF-β1, PAI-1, and FN1 but in a manner that is independent of its host gene. In addition, regulation of miR-1207-5p expression by glucose and TGFβ1 is independent of PVT1. These results provide evidence supporting important roles for miR-1207-5p and its host gene in the complex pathogenesis of diabetic nephropathy.
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            Author and article information

            Journal
            PLoS One
            PLoS ONE
            plos
            plosone
            PLoS ONE
            Public Library of Science (San Francisco, CA USA )
            1932-6203
            9 December 2016
            2016
            : 11
            : 12
            : e0168353
            Article
            PONE-D-16-47640
            10.1371/journal.pone.0168353
            5148166
            27936176
            7944760b-c6c5-47e9-8587-bbea1d5f973f
            © 2016 Alvarez et al

            This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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