Hua Zhu1, Jincai Hou2, Janet L Roe3, Ki Ho Park1, Tao Tan4, Yongqiu Zheng2, Lei Li2, Cuixiang Zhang2, Jianxun Liu2, Zhenguo Liu5, Jianjie Ma1,4, Thomas J Walters3. 1. Department of Surgery, Davis Heart and Lung Research Institute, The Ohio State University Wexner Medical Center, Columbus, Ohio, USA. 2. The Laboratory Research Center of Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, 100091, P.R. China. 3. US Army Institute of Surgical Research, Extremity Trauma and Regenerative Medicine, Fort Sam Houston, Texas, 78234, USA. 4. Division of Protein Therapeutics, TRIM-edicine, Inc., Columbus, Ohio, USA. 5. Department of Internal Medicine, Davis Heart and Lung Research Institute, The Ohio State University Wexner Medical Center, Columbus, Ohio, USA.
Abstract
INTRODUCTION: Ischemia-reperfusion injury (I-R) in skeletal muscle requires timely treatment. METHODS: Rodent models of I-R injury were used to test the efficacy of recombinant human MG53 (rhMG53) protein for protecting skeletal muscle. RESULTS: In a mouse I-R injury model, we found that mg53,-/- mice are more susceptible to I-R injury. rhMG53 applied intravenously to the wild-type mice protected I-R injured muscle, as demonstrated by reduced CK release and Evans blue staining. Histochemical studies confirmed beneficial effects of rhMG53. Of interest, rhMG53 did not protect against I-R injury in rat skeletal muscle. This was likely due to the fact that the plasma level of endogenous MG53 protein is high in rats. CONCLUSIONS: Our data suggest that rhMG53 may be a potential therapy for protection against muscle trauma. A mouse model appears to be a better choice than a rat model for evaluating potential treatments for protecting skeletal muscle.
INTRODUCTION:Ischemia-reperfusion injury (I-R) in skeletal muscle requires timely treatment. METHODS: Rodent models of I-R injury were used to test the efficacy of recombinant humanMG53 (rhMG53) protein for protecting skeletal muscle. RESULTS: In a mouse I-R injury model, we found that mg53,-/- mice are more susceptible to I-R injury. rhMG53 applied intravenously to the wild-type mice protected I-R injured muscle, as demonstrated by reduced CK release and Evans blue staining. Histochemical studies confirmed beneficial effects of rhMG53. Of interest, rhMG53 did not protect against I-R injury in rat skeletal muscle. This was likely due to the fact that the plasma level of endogenous MG53 protein is high in rats. CONCLUSIONS: Our data suggest that rhMG53 may be a potential therapy for protection against muscle trauma. A mouse model appears to be a better choice than a rat model for evaluating potential treatments for protecting skeletal muscle.
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