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      Erratum: Treatment of Dystrophic mdx Mice with an ADAMTS-5 Specific Monoclonal Antibody Increases the Ex Vivo Strength of Isolated Fast Twitch Hindlimb Muscles. Biomolecules 2020, 10, 416

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          Abstract

          The authors wish to make a change to this published paper [1]. In the original manuscript, there was a mistake in the labeling of the y-axis for Figure 5B,D. To assess muscle fatiguability, extensor digitorum longus (EDL) and soleus muscles were subjected to 4 min of intermittent (1 contraction every 5 s), submaximal stimulation at 60 Hz. The force output of every fifth contraction is statistically presented as a data point. The revision to Figure 5B,D now reflects the correct stimulation number. The authors apologize for any inconvenience caused, and we wish to stress that this change does not affect the presented scientific results and statistical analyses. The manuscript with be updated and the original will remain online on the article webpage at https://www.mdpi.com/2218-273X/10/3/416.

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          Treatment of Dystrophic mdx Mice with an ADAMTS-5 Specific Monoclonal Antibody Increases the Ex Vivo Strength of Isolated Fast Twitch Hindlimb Muscles

          Aberrant extracellular matrix synthesis and remodeling contributes to muscle degeneration and weakness in Duchenne muscular dystrophy (DMD). ADAMTS-5, a secreted metalloproteinase with catalytic activity against versican, is implicated in myogenesis and inflammation. Here, using the mdx mouse model of DMD, we report increased ADAMTS-5 expression in dystrophic hindlimb muscles, localized to regions of regeneration and inflammation. To investigate the pathophysiological significance of this, 4-week-old mdx mice were treated with an ADAMTS-5 monoclonal antibody (mAb) or IgG2c (IgG) isotype control for 3 weeks. ADAMTS-5 mAb treatment did not reduce versican processing, as protein levels of the cleaved versikine fragment did not differ between hindlimb muscles from ADAMTS-5 mAb or IgG treated mdx mice. Nonetheless, ADAMTS-5 blockade improved ex vivo strength of isolated fast extensor digitorum longus, but not slow soleus, muscles. The underpinning mechanism may include modulation of regenerative myogenesis, as ADAMTS-5 blockade reduced the number of recently repaired desmin positive myofibers without affecting the number of desmin positive muscle progenitor cells. Treatment with the ADAMTS-5 mAb did not significantly affect markers of muscle damage, inflammation, nor fiber size. Altogether, the positive effects of ADAMTS-5 blockade in dystrophic muscles are fiber-type-specific and independent of versican processing.
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            Author and article information

            Journal
            Biomolecules
            Biomolecules
            biomolecules
            Biomolecules
            MDPI
            2218-273X
            15 July 2020
            July 2020
            15 July 2020
            : 10
            : 7
            : 1053
            Affiliations
            [1 ]Centre for Molecular and Medical Research, School of Medicine, Deakin University, Waurn Ponds, VIC 3216, Australia; alex.addinsall@ 123456ki.se (A.B.A.); leonard.forgan@ 123456deakin.edu.au (L.G.F.); natasha.mcrae1@ 123456deakin.edu.au (N.L.M.); rwkelly@ 123456deakin.edu.au (R.W.K.); penny.mcdonald@ 123456mcri.edu.au (P.L.M.); bryony.mcneill@ 123456deakin.edu.au (B.M.); daniel.mcculloch@ 123456uq.net.au (D.R.M.)
            [2 ]Department of Physiology and Pharmacology, Karolinska Insitutet, 171 77 Stockholm, Sweden
            [3 ]Department of Medicine—Western Health, The University of Melbourne, St. Albans, VIC 3021, Australia
            [4 ]Australian Institute for Musculoskeletal Science (AIMSS), 176 Furlong Road, St. Albans, VIC 3021, Australia
            Author notes
            [* ]Correspondence: nicole.stupka@ 123456unimelb.edu.au ; Tel.: +613-8395-8228
            [†]

            Authors contributed equally.

            Article
            biomolecules-10-01053
            10.3390/biom10071053
            7408084
            32679807
            dc9c798b-0ea0-4f01-8a89-b780c53334bc
            © 2020 by the authors.

            Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

            History
            : 09 July 2020
            : 10 July 2020
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