Expression of matrix metalloproteinases, inhibitor, and acid phosphatase in muscles of immobilized hindlimbs of rats

Reznick, Abraham Z.; Menashe, Ofir; Bar-Shai, Marina; Coleman, Raymond; Carmeli, Eli

doi:10.1002/mus.10277

Cited by 46 publications

(59 citation statements)

References 35 publications

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“…Recent studies suggest that MMPs play an important role in response to muscle injury and repair (57) and rats under long-term hindlimb suspension have increased MMP2 activity (52). Our studies suggest that MMPs have differential activity in cast-immobilized and tenotomy-treated muscles.…”

Section: Discussionmentioning

confidence: 51%

Distinct protein degradation profiles are induced by different disuse models of skeletal muscle atrophy

Bialek

Morris

Parkington

et al. 2011

Physiological Genomics

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Section: Discussionmentioning

confidence: 51%

Distinct protein degradation profiles are induced by different disuse models of skeletal muscle atrophy

Bialek

Morris

Parkington

et al. 2011

Physiological Genomics

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“…The majority of studies regarding skeletal muscle protein degradation during disuse atrophy have focused on three primary proteolytic pathways: the cytosolic Ca 2ϩ -dependent proteolysis (calpains), lysosomal proteolysis (cathepsins), and ATP-dependent proteolysis (ubiquitin-proteasome degradation). Nevertheless, other degradative processes including intracellular and extracellular protease cascades (serine proteases and matrix metalloproteinases) and apoptosis (caspases) are all likely involved in muscle atrophy, though with unclear extents of involvement (86,87). Recent investigations have indicated that the three primary proteolytic systems may work as partners during muscle proteolysis (17,55).…”

Section: 2) Regulation Of Protein Degradationmentioning

confidence: 99%

Determinants of Disuse-Induced Skeletal Muscle Atrophy: Exercise and Nutrition Countermeasures to Prevent Protein Loss

Bajotto

Shimomura

2006

J Nutr Sci Vitaminol

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Summary Muscle atrophy results from a variety of conditions such as disease states, neuromuscular injuries, disuse, and aging. Absence of gravitational loading during spaceflight or long-term bed rest predisposes humans to undergo substantial loss of muscle mass and, consequently, become unfit and/or unhealthy. Disuse-or inactivity-induced skeletal muscle protein loss takes place by differential modulation of proteolytic and synthetic systems. Transcriptional, translational, and posttranslational events are involved in the regulation of protein synthesis and degradation in myofibers, and these regulatory events are known to be responsive to contractile activity. However, regardless of the numerous studies which have been performed, the intracellular signals that mediate skeletal muscle wasting due to muscular disuse are not completely comprehended. Understanding the triggers of atrophy and the mechanisms that regulate protein loss in unloaded muscles may lead to the development of effective countermeasures such as exercise and dietary intervention. The objective of the present review is to provide a window into the molecular processes that underlie skeletal muscle remodeling and to examine what we know about exercise and nutrition countermeasures designed to minimize muscle atrophy. Key Words Skeletal muscle disuse atrophy, microgravity, hindlimb suspension, protein synthesis and degradation, exercise and nutrition countermeasures Because skeletal muscle is the most abundant tissue of the human body, we may hypothesize that decreases in its mass possibly will profoundly impact the wholebody metabolism and ultimately lead to the development of lifestyle-related diseases. In addition, muscle deconditioning (reduced strength, abnormal reflex patterns, increased fatigability) could limit the ability of astronauts to work in space and/or to rapidly egress the spacecraft in an emergency landing ( 1 ). Even though various functional and morphological alterations are noticeable in inactive muscles, decreased protein content has been regarded as the hallmark of skeletal muscle atrophy. Muscle protein can be either gained or lost by relative changes in protein synthesis and degradation rates, which are known to be modulated by contractile activity. Thus, understanding about the molecular regulators of protein turnover during different mechanical loading conditions and their response to specific treatments leads to the likelihood of developing effective countermeasures for preventing disuseinduced muscle wasting.This article provides a review of muscular adaptations to disuse, with emphasis on protein kinetics. We describe first the general aspects of muscle wasting with regard to exposure to actual or ground-based, simulated microgravity and some of the most significant findings that provide evidence for a close connection between skeletal muscle plasticity and protein metabolism. Next, we present a review of the literature in which results of measurements of protein synthesis/ degradation rates during unloading are avail...

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“…1 Recent studies suggest that matrix metalloproteinase-2 (MMP-2) plays a key role in the response of muscle tissue to various forms of injury and disuse. [2][3][4][5] However, the mechanisms of MMP-2 regulation associated with muscle atrophy remain undefined.…”

Section: Introductionmentioning

confidence: 99%

Matrix metalloproteinase‐2 expression and promoter/enhancer activity in skeletal muscle atrophy

Skittone

Liu

Tseng

et al. 2007

Journal Orthopaedic Research

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Matrix metalloproteinase-2 (MMP-2) appears to be the dominant MMP activated during skeletal muscle atrophy. However, little is known about cell-specific regulatory mechanisms of MMP-2 transcription in vivo. In this study, we used a mouse model of muscle atrophy induced by complete Achilles tendon transection. Time-dependent muscle weight loss, nuclei density reduction, and extracellular matrix degeneration were observed consistently after Achilles tendon transection. Increased MMP-2 expression was confirmed at the mRNA and protein level. Experiments using transgenic mice with a MMP-2 promoter/enhancer reporter construct demonstrated markedly increased MMP-2 promoter/enhancer activity in atrophic skeletal muscle. Tissue-specific upregulation of MMP-2 promoter activity was observed not only in myocytes, but also in blood vessels, nerve, and fascia. The transcription factors c-Jun and FosB were expressed at high levels in atrophic muscle, suggesting a role in MMP-2 upregulation. These findings show that increased MMP-2 activity in disused atrophic muscle and supporting tissues is regulated, at least in part, by increased MMP-2 promoter/enhancer activity. ß

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Expression of matrix metalloproteinases, inhibitor, and acid phosphatase in muscles of immobilized hindlimbs of rats

Cited by 46 publications

References 35 publications

Distinct protein degradation profiles are induced by different disuse models of skeletal muscle atrophy

Distinct protein degradation profiles are induced by different disuse models of skeletal muscle atrophy

Determinants of Disuse-Induced Skeletal Muscle Atrophy: Exercise and Nutrition Countermeasures to Prevent Protein Loss

Matrix metalloproteinase‐2 expression and promoter/enhancer activity in skeletal muscle atrophy

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