Poloxamer 188 reduces the contraction-induced force decline in lumbrical muscles from <i>mdx</i> mice

Ng, Rainer; Metzger, Joseph M.; Claflin, Dennis R.; Faulkner, John A.

doi:10.1152/ajpcell.00017.2008

Cited by 54 publications

(40 citation statements)

References 35 publications

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“…Exposure of muscles of mdx mice to either calcium-free buffer or buffer supplemented with the antioxidant N-acetylcysteine (NAC) decreased contraction-induced force deficits to 50% of those in control buffer (Fig. 3A and Table S2), confirming earlier reports regarding mdx mice (28)(29)(30)(31). In contrast, muscles of inducible DG KO mice were unresponsive to the conditions of calcium-free buffer and antioxidant supplementation (Fig.…”

Section: Evidence Of Titin Disruption Rather Than Increased Sarcolemmsupporting

confidence: 88%

“…In dystrophic muscles, damage mediated by extracellular calcium or reactive oxygen species is a consequence of increased membrane permeability (28)(29)(30). Exposure of muscles of mdx mice to either calcium-free buffer or buffer supplemented with the antioxidant N-acetylcysteine (NAC) decreased contraction-induced force deficits to 50% of those in control buffer (Fig.…”

Section: Evidence Of Titin Disruption Rather Than Increased Sarcolemmmentioning

confidence: 99%

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Role of dystroglycan in limiting contraction-induced injury to the sarcomeric cytoskeleton of mature skeletal muscle

Rader

Turk

Willer

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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Dystroglycan (DG) is a highly expressed extracellular matrix receptor that is linked to the cytoskeleton in skeletal muscle. DG is critical for the function of skeletal muscle, and muscle with primary defects in the expression and/or function of DG throughout development has many pathological features and a severe muscular dystrophy phenotype. In addition, reduction in DG at the sarcolemma is a common feature in muscle biopsies from patients with various types of muscular dystrophy. However, the consequence of disrupting DG in mature muscle is not known. Here, we investigated muscles of transgenic mice several months after genetic knockdown of DG at maturity. In our study, an increase in susceptibility to contractioninduced injury was the first pathological feature observed after the levels of DG at the sarcolemma were reduced. The contractioninduced injury was not accompanied by increased necrosis, excitation-contraction uncoupling, or fragility of the sarcolemma. Rather, disruption of the sarcomeric cytoskeleton was evident as reduced passive tension and decreased titin immunostaining. These results reveal a role for DG in maintaining the stability of the sarcomeric cytoskeleton during contraction and provide mechanistic insight into the cause of the reduction in strength that occurs in muscular dystrophy after lengthening contractions. muscular dystrophy | eccentric contraction | titin | skeletal muscle | dystroglycan

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Section: Evidence Of Titin Disruption Rather Than Increased Sarcolemmsupporting

confidence: 88%

Section: Evidence Of Titin Disruption Rather Than Increased Sarcolemmmentioning

confidence: 99%

Role of dystroglycan in limiting contraction-induced injury to the sarcomeric cytoskeleton of mature skeletal muscle

Rader

Turk

Willer

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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“…Such defects at the membrane are thought to either directly or indirectly contribute to the observed degeneration of myofibers that ultimately results in impaired muscle function and weakness. The increased fragility of the sarcolemma in mdx mice is also supported by the observation that treatment with membrane sealants in vitro leads to a decrease in the magnitude of injury produced by repetitive isometric contractions (41). Therefore, susceptibility to contraction-induced injury appears to be a hallmark feature in many forms of DGC-related muscular dystrophy.…”

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confidence: 82%

Soleus muscle in glycosylation-deficient muscular dystrophy is protected from contraction-induced injury

Gumerson

Kabaeva

Davis

et al. 2010

American Journal of Physiology-Cell Physiology

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The glycosylation of dystroglycan is required for its function as a high-affinity laminin receptor, and loss of dystroglycan glycosylation results in congenital muscular dystrophy. The purpose of this study was to investigate the functional defects in slow- and fast-twitch muscles of glycosylation-deficient Large(myd) mice. While a partial alteration in glycosylation of dystroglycan in heterozygous Large(myd/+) mice was not sufficient to alter muscle function, homozygous Large(myd/myd) mice demonstrated a marked reduction in specific force in both soleus and extensor digitorum longus (EDL) muscles. Although EDL muscles from Large(myd/myd) mice were highly susceptible to lengthening contraction-induced injury, Large(myd/myd) soleus muscles surprisingly showed no greater force deficit compared with wild-type soleus muscles even after five lengthening contractions. Despite no increased susceptibility to injury, Large(myd/myd) soleus muscles showed loss of dystroglycan glycosylation and laminin binding activity and dystrophic pathology. Interestingly, we show that soleus muscles have a markedly higher sarcolemma expression of β(1)-containing integrins compared with EDL and gastrocnemius muscles. Therefore, we conclude that β(1)-containing integrins play an important role as matrix receptors in protecting muscles containing slow-twitch fibers from contraction-induced injury in the absence of dystroglycan function, and that contraction-induced injury appears to be a separable phenotype from the dystrophic pathology of muscular dystrophy.

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“…Developing a way to protect muscle fiber membranes from stretch-induced injury potentially could prevent some of the difficulties of failed repairs or continued progression of fatty degeneration that is observed at times in patients who undergo rotator cuff repair. Membrane sealing molecules like poloxamer 188 [21] or pharmaceutical compounds that upregulate endogenous membrane sealing proteins like dysferlin [15] could help to protect muscles from lengthening injury after rotator cuff repair, and warrant further study in preclinical models of rotator cuff tear.…”

Section: Discussionmentioning

confidence: 99%

Muscle Fibers are Injured at the Time of Acute and Chronic Rotator Cuff Repair

Davis

Stafford

Jergenson

et al. 2015

Clinical Orthopaedics &Amp; Related Research

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In this animal model, we found that repair of chronically torn cuff muscles results in extensive injury throughout the muscle. Based on these findings, we posit that inducing a widespread injury at the time of surgical repair of chronically torn rotator cuff muscles may contribute to the problems of failed repairs or continued progression of fatty degeneration that is observed in some patients that undergo rotator cuff repair. Therapeutic interventions to protect muscle fiber membranes potentially could enhance outcomes for patients undergoing rotator cuff repair. To evaluate this, future studies that evaluate the use of membrane sealing compounds or drugs that upregulate endogenous membrane-sealing proteins are warranted.

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Poloxamer 188 reduces the contraction-induced force decline in lumbrical muscles from mdx mice

Abstract: Ng R, Metzger JM, Claflin DR, Faulkner JA. Poloxamer 188 reduces the contraction-induced force decline in lumbrical muscles from mdx mice.

Cited by 54 publications

References 35 publications

Role of dystroglycan in limiting contraction-induced injury to the sarcomeric cytoskeleton of mature skeletal muscle

Role of dystroglycan in limiting contraction-induced injury to the sarcomeric cytoskeleton of mature skeletal muscle

Soleus muscle in glycosylation-deficient muscular dystrophy is protected from contraction-induced injury

Muscle Fibers are Injured at the Time of Acute and Chronic Rotator Cuff Repair

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