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      Correction: Magic-Factor 1, a Partial Agonist of Met, Induces Muscle Hypertrophy by Protecting Myogenic Progenitors from Apoptosis

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          Abstract

          After publication of this article [1], the following concerns were raised about the figures: Figure 2E follistatin and GAPDH panels contain background irregularities such that lane 1 appears to have a different background to lanes 2–6; Figure 3B Magic-F1 and HGF panels contain background irregularities such that lanes 1–3 appear to have a different background to lanes 4–6; Fig 5A WT 3d and WT 7d panels appear similar. Regarding Fig 5A, the authors clarify that the bottom images at 3d and 7d for WT have been erroneously swapped. In the published paper the image below 3d should be below 7d, and vice versa. This is a double IF analysis to test embryonic myosin (red) and laminin (green). Thus all WT upper panels are same images of below using a different light channel. The authors have provided the original images used in Figures 2E and 3B. The original images do not contain background irregularities and the source of the image artifact is unclear. With this correction, the authors provide an updated Fig 5, along with the original images underlying Figs 5A, 2E, and 3B (in Supporting Information S1 File). 10.1371/journal.pone.0220357.g001 Fig 5 Magic-F1 promotes muscular regeneration. (A) Immunofluorescence analysis of muscle fibers using antibodies against embryonic myosin heavy chain (red) or laminin (green) in the tibialis anterior of transgenic and wild-type mice. Nuclei were stained with DAPI. (B) Immunofluorescence analysis for desmin (middle panels, in green) and myosin heavy chain (lower panels, in red) of satellite cells isolated from tibialis anterior of Magic-F1 transgenic mice (M) and wild-type (WT) mice subjected to cardiotoxin treatment. Nuclei are stained with DAPI (in blue). The upper panels show a phase contrast image of satellite cell clones, 3 days after low density seeding. (C) TUNEL analysis of tibialis anterior after 3, 7 and 14 days after cardiotoxin treatment. (D) Quantification of apoptotic nuclei (ap nuclei) relative to the experiment described in C. Red line, transgenic mice; blue line, wild-type mice. (E) RT-PCR analysis of myogenic transcription factor expression (MyoD and Myf5) conducted on tibialis anterior from transgenic (M) or wild-type (WT) mice. (F) Representative images of tibialis anterior muscles stained with H&E extracted from Magic-F1 transgenic mice and wild-type mice 10 days after cardiotoxin treatment. Note the larger size of fibers in the Magic-F1 group (M) compared to the control group (WT). Supporting information S1 File Original raw images for Figs 5A, 2E, and 3B. (ZIP) Click here for additional data file.

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          Magic-Factor 1, a Partial Agonist of Met, Induces Muscle Hypertrophy by Protecting Myogenic Progenitors from Apoptosis

          Background Hepatocyte Growth Factor (HGF) is a pleiotropic cytokine of mesenchymal origin that mediates a characteristic array of biological activities including cell proliferation, survival, motility and morphogenesis. Its high affinity receptor, the tyrosine kinase Met, is expressed by a wide range of tissues and can be activated by either paracrine or autocrine stimulation. Adult myogenic precursor cells, the so called satellite cells, express both HGF and Met. Following muscle injury, autocrine HGF-Met stimulation plays a key role in promoting activation and early division of satellite cells, but is shut off in a second phase to allow myogenic differentiation. In culture, HGF stimulation promotes proliferation of muscle precursors thereby inhibiting their differentiation. Methodology/Principal Findings Magic-Factor 1 (Met-Activating Genetically Improved Chimeric Factor-1 or Magic-F1) is an HGF-derived, engineered protein that contains two Met-binding domains repeated in tandem. It has a reduced affinity for Met and, in contrast to HGF it elicits activation of the AKT but not the ERK signaling pathway. As a result, Magic-F1 is not mitogenic but conserves the ability to promote cell survival. Here we show that Magic-F1 protects myogenic precursors against apoptosis, thus increasing their fusion ability and enhancing muscular differentiation. Electrotransfer of Magic-F1 gene into adult mice promoted muscular hypertrophy and decreased myocyte apoptosis. Magic-F1 transgenic mice displayed constitutive muscular hypertrophy, improved running performance and accelerated muscle regeneration following injury. Crossing of Magic-F1 transgenic mice with α-sarcoglycan knock-out mice –a mouse model of muscular dystrophy– or adenovirus-mediated Magic-F1 gene delivery resulted in amelioration of the dystrophic phenotype as measured by both anatomical/histological analysis and functional tests. Conclusions/Significance Because of these features Magic-F1 represents a novel molecular tool to counteract muscle wasting in major muscular diseases such as cachexia or muscular dystrophy.
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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
            24 July 2019
            2019
            24 July 2019
            : 14
            : 7
            Article
            PONE-D-19-20060
            10.1371/journal.pone.0220357
            6655771
            31339946
            © 2019 Cassano 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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