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Effect of recombinant human MG53 protein on tourniquet-induced ischemia-reperfusion injury in rat muscle.


ABSTRACT:

Introduction

Skeletal muscle ischemia-reperfusion injury (I-R) is a complex injury process that includes damage to the sarcolemmal membrane, contributing to necrosis and apoptosis. MG53, a muscle-specific TRIM family protein, has been shown to be essential for regulating membrane repair and has been shown to be protective against cardiac I-R and various forms of skeletal muscle injury. The purpose of this study was to determine if recombinant human MG53 (rhMG53) administration offered protection against I-R.

Methods

rhMG53 was administered to rats immediately before tourniquet-induced ischemia and again immediately before reperfusion. Two days later muscle damage was assessed histologically.

Results

rhMG53 offered no protective effect, as evidenced primarily by similar Evans blue dye inclusion in the muscles of rats administered rhMG53 or saline.

Conclusions

Administration of rhMG53 does not offer protection against I-R in rat skeletal muscle. Additional studies are required to determine if the lack of a response is species-specific.

SUBMITTER: Corona BT 

PROVIDER: S-EPMC4028410 | biostudies-literature | 2014 Jun

REPOSITORIES: biostudies-literature

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Effect of recombinant human MG53 protein on tourniquet-induced ischemia-reperfusion injury in rat muscle.

Corona Benjamin T BT   Garg Koyal K   Roe Janet L JL   Zhu Hua H   Park Ki Ho KH   Ma Jianjie J   Walters Thomas J TJ  

Muscle & nerve 20140601 6


<h4>Introduction</h4>Skeletal muscle ischemia-reperfusion injury (I-R) is a complex injury process that includes damage to the sarcolemmal membrane, contributing to necrosis and apoptosis. MG53, a muscle-specific TRIM family protein, has been shown to be essential for regulating membrane repair and has been shown to be protective against cardiac I-R and various forms of skeletal muscle injury. The purpose of this study was to determine if recombinant human MG53 (rhMG53) administration offered pr  ...[more]

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