Increased muscle expression of interleukin-17 in Duchenne muscular dystrophy

Pasquale, Loredana De; D’Amico, Adele; Verardo, Margherita; Petrini, Stefania; Bertini, Enrico; Benedetti, Fabrizio

doi:10.1212/wnl.0b013e3182518302

Cited by 42 publications

(30 citation statements)

References 40 publications

(32 reference statements)

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“…IL17a is described as a proinflammatory cytokine that is produced by a subset of T cells known as helper T 17 cells (Torchinsky and Blander, 2010). IL17a has been found to be upregulated in Duchenne muscular dystrophy and has been demonstrated to negatively affect myoblast migration and terminal differentiation (De Pasquale et al, 2012;Kocic et al, 2013). Furthermore, another group has postulated that IL17, which is induced by IL6 and activated by IL23, might have a significant contribution in promoting activation of neutrophils and ensuing muscle damage following prolonged endurance exercise (Sugama et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

Follistatin: A Novel Therapeutic for the Improvement of Muscle Regeneration

Yaden

Croy²,

Wang³

et al. 2014

J Pharmacol Exp Ther

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Follistatin (FST) is a member of the tissue growth factor b family and is a secreted glycoprotein that antagonizes many members of the family, including activin A, growth differentiation factor 11, and myostatin. The objective of this study was to explore the use of an engineered follistatin therapeutic created by fusing FST315 lacking heparin binding activity to the N terminus of a murine IgG1 Fc (FST315-DHBS-Fc) as a systemic therapeutic agent in models of muscle injury. Systemic administration of this molecule was found to increase body weight and lean muscle mass after weekly administration in normal mice. Subsequently, we tested this agent in several models of muscle injury, which were chosen based on their severity of damage and their ability to reflect clinical settings. FST315-DHBS-Fc treatment proved to be a potent inducer of muscle remodeling and regeneration. FST315-DHBS-Fc induced improvements in muscle repair after injury/atrophy by modulating the early inflammatory phase allowing for increased macrophage density, and Pax7-positive cells leading to an accelerated restoration of myofibers and muscle function. Collectively, these data demonstrate the benefits of a therapeutically viable form of FST that can be leveraged as an alternate means of ameliorating muscle regeneration.

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Section: Discussionmentioning

confidence: 99%

Follistatin: A Novel Therapeutic for the Improvement of Muscle Regeneration

Yaden

Croy²,

Wang³

et al. 2014

J Pharmacol Exp Ther

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“…The IL-17 family has been implicated in several autoimmune diseases including multiple sclerosis (MS), RA and inflammatory bowel disease 75; 76 . Recent studies have shown that IL-17 mRNA is elevated in muscle biopsies from Duchenne muscular dystrophy (DMD) patients suggesting a possible pathogenic role 77 .…”

Section: Mediators Of Inflammationmentioning

confidence: 99%

Inflammation induced loss of skeletal muscle

Londhe

Guttridge

2015

Bone

218

180

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“…The pathophysiology of DMD involves many secondary changes (Gorospe et al, 1994;Chen et al, 2000;Head, 2010;Altamirano et al, 2012;De Pasquale et al, 2012;Gehrig et al, 2012) owing to mutation in the dystrophin gene. This high complex progression of DMD presents challenges for curing the disease.…”

Section: Discussionmentioning

confidence: 99%

“…Understanding the pathomechanisms for DMD may lead to alternatives to currently inadequate therapeutic strategies. Previous studies have shown that DMD patients exhibit symptoms related to various proteins or molecules, such as growth factors (Gehrig et al, 2012), nitric oxide synthase (Altamirano et al, 2012), phospholipase (Lindahl et al, 1995), and cytokines (De Pasquale et al, 2012), suggesting that "molecule groups" instead of single or a few proteins should be explored in the investigation of the DMD pathomechanism. Protein-protein interaction (PPI) is crucial for all biological processes (Stelzl et al, 2005) because the majority of proteins function with other proteins.…”

Section: Introductionmentioning

confidence: 99%

Analysis of differentially expressed genes in various stages of Duchenne muscular dystrophy by using a network view

Wang

Wang²,

Song³

et al. 2013

Genet. Mol. Res.

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ABSTRACT. Duchenne muscular dystrophy (DMD), which is caused by mutations in the X-linked dystrophin gene, is a severe and progressive neuromuscular disease with no available cure. By integrating 2 microarray datasets from the Gene Expression Omnibus, we identified differentially expressed genes in 2 stages of DMD and systematically explored their potential disease-related mechanisms using a network view. Twenty differentially expressed genes were detected in various stages of DMD. According to the network with dystrophin as its center, none of the 20 proteins interacts with dystrophin directly. IQ motif-containing GTPaseactivating protein 1 was found in the 2nd-level neighbors with a degree of 21. Microtubule-associated protein tau, membrane metallo-endopeptidase, interleukin 13 receptor alpha 1, and multiple epidermal growth factor-like domains 6 were found in the 3rd-level neighbors. These identifications require further investigation, as this report is the first of possible associations between DMD and these proteins. Analysis of differentially expressed genes through this network view may provide important information for further exploration of underlying mechanisms of DMD.

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Increased muscle expression of interleukin-17 in Duchenne muscular dystrophy

Cited by 42 publications

References 40 publications

Follistatin: A Novel Therapeutic for the Improvement of Muscle Regeneration

Follistatin: A Novel Therapeutic for the Improvement of Muscle Regeneration

Inflammation induced loss of skeletal muscle

Analysis of differentially expressed genes in various stages of Duchenne muscular dystrophy by using a network view

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