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      Expression of diaphragmatic myostatin and correlation with apoptosis in rats with chronic obstructive pulmonary disease

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          Abstract

          Chronic obstructive pulmonary disease (COPD) is characterized by progressive airflow limitation and loss of lung function. The present study aimed to investigate the diaphragmatic protein expression of myostatin and its correlation with apoptosis in a rat model of CPOD. Sprague Dawley rats were randomly divided into a control group and a COPD group, the latter of which were exposed to cigarette smoke to build a rat model of COPD. The validity of the COPD model was evaluated by assessment of lung function and histopathological analysis. Diaphragmatic myostatin expression and apoptosis were measured by western blot and terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick end labeling, respectively. The rat model of COPD was efficiently established by cigarette smoke exposure. Diaphragmatic myostatin expression and apoptotic index in COPD rats were obviously increased as compared with that in the control animals. A positive correlation between diaphragmatic myostatin expression and apoptotic index was identified (r=0.857). Diaphragmatic myostatin overexpression in rats with COPD may promote diaphragmatic apoptosis and atrophy, leading to diaphragm weakness and respiratory muscle dysfunction, which is involved in the pathology of COPD.

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          Glucocorticoid-induced skeletal muscle atrophy is associated with upregulation of myostatin gene expression.

          Vahid Pirhajati Mahabadi, Shalender Bhasin, Jorge N. Artaza … (2003)
          The mechanisms by which excessive glucocorticoids cause muscular atrophy remain unclear. We previously demonstrated that dexamethasone increases the expression of myostatin, a negative regulator of skeletal muscle mass, in vitro. In the present study, we tested the hypothesis that dexamethasone-induced muscle loss is associated with increased myostatin expression in vivo. Daily administration (60, 600, 1,200 micro g/kg body wt) of dexamethasone for 5 days resulted in rapid, dose-dependent loss of body weight (-4.0, -13.4, -17.2%, respectively, P < 0.05 for each comparison), and muscle atrophy (6.3, 15.0, 16.6% below controls, respectively). These changes were associated with dose-dependent, marked induction of intramuscular myostatin mRNA (66.3, 450, 527.6% increase above controls, P < 0.05 for each comparison) and protein expression (0.0, 260.5, 318.4% increase above controls, P < 0.05). We found that the effect of dexamethasone on body weight and muscle loss and upregulation of intramuscular myostatin expression was time dependent. When dexamethasone treatment (600 micro g. kg-1. day-1) was extended from 5 to 10 days, the rate of body weight loss was markedly reduced to approximately 2% within this extended period. The concentrations of intramuscular myosin heavy chain type II in dexamethasone-treated rats were significantly lower (-43% after 5-day treatment, -14% after 10-day treatment) than their respective corresponding controls. The intramuscular myostatin concentration in rats treated with dexamethasone for 10 days returned to basal level. Concurrent treatment with RU-486 blocked dexamethasone-induced myostatin expression and significantly attenuated body loss and muscle atrophy. We propose that dexamethasone-induced muscle loss is mediated, at least in part, by the upregulation of myostatin expression through a glucocorticoid receptor-mediated pathway.
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            TGFβ and BMP signaling in skeletal muscle: potential significance for muscle-related disease.

            Roberta Sartori, Paul Gregorevic, Marco Sandri (2014)
            The transforming growth factor beta (TGFβ) superfamily comprises a large number of secreted proteins that regulate various fundamental biological processes underlying embryonic development and the postnatal regulation of many cell types and organs. Sequence similarities define two ligand subfamilies: the TGFβ/activin subfamily and the bone morphogenetic protein (BMP) subfamily. The discovery that myostatin, a member of the TGFβ/activin subfamily, negatively controls muscle mass attracted attention to this pathway. However, recent findings of a positive role for BMP-mediated signaling in muscle have challenged the model of how the TGFβ network regulates skeletal muscle phenotype. This review illustrates how this complex network integrates crosstalk among members of the TGFβ superfamily and downstream signaling elements to regulate muscle in health and disease.
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              Pathophysiology of muscle dysfunction in COPD.

              Josep Roca, Joaquim Gea, Àlvar Agustí (2013)
              Muscle dysfunction often occurs in patients with chronic obstructive pulmonary disease (COPD) and may involve both respiratory and locomotor (peripheral) muscles. The loss of strength and/or endurance in the former can lead to ventilatory insufficiency, whereas in the latter it limits exercise capacity and activities of daily life. Muscle dysfunction is the consequence of complex interactions between local and systemic factors, frequently coexisting in COPD patients. Pulmonary hyperinflation along with the increase in work of breathing that occur in COPD appear as the main contributing factors to respiratory muscle dysfunction. By contrast, deconditioning seems to play a key role in peripheral muscle dysfunction. However, additional systemic factors, including tobacco smoking, systemic inflammation, exercise, exacerbations, nutritional and gas exchange abnormalities, anabolic insufficiency, comorbidities and drugs, can also influence the function of both respiratory and peripheral muscles, by inducing modifications in their local microenvironment. Under all these circumstances, protein metabolism imbalance, oxidative stress, inflammatory events, as well as muscle injury may occur, determining the final structure and modulating the function of different muscle groups. Respiratory muscles show signs of injury as well as an increase in several elements involved in aerobic metabolism (proportion of type I fibers, capillary density, and aerobic enzyme activity) whereas limb muscles exhibit a loss of the same elements, injury, and a reduction in fiber size. In the present review we examine the current state of the art of the pathophysiology of muscle dysfunction in COPD.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Exp Ther Med
                Journal ID (iso-abbrev): Exp Ther Med
                Journal ID (publisher-id): ETM
                Title: Experimental and Therapeutic Medicine
                Publisher: D.A. Spandidos
                ISSN (Print): 1792-0981
                ISSN (Electronic): 1792-1015
                Publication date (Print): March 2018
                Publication date (Electronic): 02 January 2018
                Publication date PMC-release: 02 January 2018
                Volume: 15
                Issue: 3
                Pages: 2295-2300
                Affiliations
                [1 ]Department of Critical Care Medicine, Hunan Provincial People's Hospital, Changsha, Hunan 410005, P.R. China
                [2 ]Department of Respiratory Medicine, Hunan Provincial People's Hospital, Changsha, Hunan 410005, P.R. China
                [3 ]Institute of Emergency Medicine, Hunan Provincial People's Hospital, Changsha, Hunan 410005, P.R. China
                Author notes
                Correspondence to: Dr Wenpu Li, Department of Respiratory Medicine, Hunan Provincial People's Hospital, 61 Jiefang West Road, Changsha, Hunan 410005, P.R. China, E-mail: csliwenpu@ 123456163.com
                Article
                Publisher ID: ETM-0-0-5686
                DOI: 10.3892/etm.2018.5686
                PMC ID: 5795556
                SO-VID: 42dae0ae-79ce-4bd9-a805-d55c654893d2
                Copyright © Copyright: © Zhou et al.
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

                History
                Date received : 12 July 2016
                Date accepted : 03 November 2017
                Categories
                Subject: Articles

                ScienceOpen disciplines: Medicine
                Keywords: chronic obstructive pulmonary disease,diaphragm,myostatin,apoptosis
                Data availability:
                ScienceOpen disciplines: Medicine
                Keywords: chronic obstructive pulmonary disease, diaphragm, myostatin, apoptosis

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