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Hyun Lee, Jung-Jin Park, Nga Nguyen, Jun Sub Park, Jin Hong, Seung-Hyeob Kim, Woon Young Song, Hak Joong Kim, Kwangman Choi, Sungchan Cho, Jae-Seon Lee, Bong-Woo Kim, Young-Gyu Ko
Mitsugumin 53 (MG53) is an E3 ligase that interacts with and ubiquitinates insulin receptor substrate-1 (IRS-1) in skeletal muscle; thus, an MG53-IRS-1 interaction disruptor (MID), which potentially sensitizes insulin signaling with an elevated level of IRS-1 in skeletal muscle, is an excellent candidate for treating insulin resistance. To screen for an MID, we developed a bimolecular luminescence complementation system using an N-terminal luciferase fragment fused with IRS-1 and a C-terminal luciferase fragment fused with an MG53 C14A mutant that binds to IRS-1 but does not have E3 ligase activity...
December 23, 2016: Journal of Biological Chemistry
Lei-Lei Ma, Fei-Juan Kong, Jun-Jie Guo, Jian-Bing Zhu, Hong-Tao Shi, Yang Li, Ren-Hua Sun, Jun-Bo Ge
Remote ischemic preconditioning (RIPC) is one of the most powerful intrinsic cardioprotective strategies discovered so far and experimental data indicate that comorbidity may interfere with the protection by RIPC. Therefore, we investigate whether RIPC-induced cardioprotection was intact in hypercholesterolemic rat hearts exposed to ischemia reperfusion in vivo. Normal or hypercholesterolemic rat hearts were exposed to 30 min of ischemia and 2 h of reperfusion, with or without RIPC, PI3K inhibitor wortmannin, MEK-ERK1/2 inhibitor PD98059, GSK3β inhibitor SB216763...
March 2017: Shock
Yan Zhang, Hong-Kun Wu, Feng-Xiang Lv, Rui-Ping Xiao
Mitsugumin 53 (MG53), also named Trim72, is a multi-functional TRIM-family protein, which is abundantly expressed in cardiac and skeletal muscle. It has been shown that MG53 not only plays important physiological roles but also acts as a crucial pathogenic factor of various diseases. First, MG53 preserves cardiac and skeletal muscle integrity via facilitating plasma membrane repair. Second, MG53 is essentially involved in cardiac ischemic preconditioning and postconditioning by activating PI3K-Akt-GSK3β and ERK1/2 cell survival signaling pathways...
August 25, 2016: Sheng Li Xue Bao: [Acta Physiologica Sinica]
Chao Wang, Hongyu Wang, Dan Wu, Jianhong Hu, Wei Wu, Yong Zhang, Xi Peng
Myopathy is a common complication of severe burn patients. One potential cause of this myopathy could be failure of the plasma membrane to undergo repair following injuries generated from toxin or exercise. The aim of this study is to assess systemic effect on muscle membrane repair deficiency in burn injury. Skeletal muscle fibers isolated from burn-injured mice were damaged with a UV laser and dye influx imaged confocally to evaluate membrane repair capacity. Membrane repair failure was also tested in burn-injured mice subjected to myotoxin or treadmill exercise...
2016: Scientific Reports
Jeffrey M Hord, Rachel Botchlett, John M Lawler
Age-related loss of skeletal muscle mass and function, referred to as sarcopenia, is mitigated by lifelong calorie restriction as well as exercise. In aged skeletal muscle fibers there is compromised integrity of the cell membrane that may contribute to sarcopenia. The purpose of this study was to determine if lifelong mild (8%) caloric restriction (CR) and lifelong CR+voluntary wheel running (WR) could ameliorate disruption of membrane scaffolding and signaling proteins during the aging process, thus maintaining a favorable, healthy membrane environment in plantaris muscle fibers...
October 2016: Experimental Gerontology
Alexis R Demonbreun, Mattia Quattrocelli, David Y Barefield, Madison V Allen, Kaitlin E Swanson, Elizabeth M McNally
Disruption of the plasma membrane often accompanies cellular injury, and in muscle, plasma membrane resealing is essential for efficient recovery from injury. Muscle contraction, especially of lengthened muscle, disrupts the sarcolemma. To define the molecular machinery that directs repair, we applied laser wounding to live mammalian myofibers and assessed translocation of fluorescently tagged proteins using high-resolution microscopy. Within seconds of membrane disruption, annexins A1, A2, A5, and A6 formed a tight repair "cap...
June 20, 2016: Journal of Cell Biology
Tao Tan, Young-Gyu Ko, Jianjie Ma
MG53 is a member of the TRIM-family protein that acts as a key component of the cell membrane repair machinery. MG53 is also an E3-ligase that ubiquinates insulin receptor substrate-1 and controls insulin signaling in skeletal muscle cells. Since its discovery in 2009, research efforts have been devoted to translate this basic discovery into clinical applications in human degenerative and metabolic diseases. This review article highlights the dual function of MG53 in cell membrane repair and insulin signaling, the mechanism that underlies the control of MG53 function, and the therapeutic value of targeting MG53 function in regenerative medicine...
August 2016: BMB Reports
Jin Hong, Jun-Sub Park, Hyun Lee, Jaemin Jeong, Hye Hyeon Yun, Hye Yun Kim, Young-Gyu Ko, Jeong-Hwa Lee
BCL-2 interacting cell death suppressor (BIS), which is ubiquitously expressed, has important roles in various cellular processes, such as apoptosis, the cellular stress response, migration and invasion and protein quality control. In particular, BIS is highly expressed in skeletal and cardiac muscles, and BIS gene mutations result in human myopathy. In this study, we show that mRNA and protein levels of BIS were markedly increased during skeletal myogenesis in C2C12 cells and mouse satellite cells. BIS knockdown did not prevent the early stage of skeletal myogenesis, but did induce muscle atrophy and a decrease in the diameter of myotubes...
April 1, 2016: Experimental & Molecular Medicine
Jianquan Zhao, Han Lei
BACKGROUND: The proliferation and migration of cardiac fibroblasts are critical for the progress of cardiac fibrosis. Tripartite motif protein 72 (Trim72), also known as MG53, mediates the dynamic process of membrane fusion and exocytosis in striated muscle. However, the role of Trim72 in the proliferation and migration of cardiac fibroblasts is unknown. METHODS: In the present study, we used small interference RNA (siRNA) to silence Trim72 and then investigated the effects of Trim72 on cardiac fibroblast proliferation and migration, which were activated during cardiac remodeling after myocardial infarction...
2016: Cardiology
Yonggang Yao, Bo Zhang, Hua Zhu, Haichang Li, Yu Han, Ken Chen, Zhen Wang, Jing Zeng, Yukai Liu, Xinquan Wang, Yu Li, Duofen He, Peihui Lin, Xinyu Zhou, Ki Ho Park, Zehua Bian, Zhishui Chen, Nianqiao Gong, Tao Tan, Jingsong Zhou, Meng Zhang, Jianjie Ma, Chunyu Zeng
Ischemic injury to neurons represents the underlying cause of stroke to the brain. Our previous studies identified MG53 as an essential component of the cell membrane repair machinery. Here we show that the recombinant human (rh)MG53 protein facilitates repair of ischemia-reperfusion (IR) injury to the brain. MG53 rapidly moves to acute injury sites on neuronal cells to form a membrane repair patch. IR-induced brain injury increases permeability of the blood-brain-barrier, providing access of MG53 from blood circulation to target the injured brain tissues...
April 19, 2016: Oncotarget
Frances A Lemckert, Adam Bournazos, Daniel M Eckert, Manuel Kenzler, Joanne M Hawkes, Tanya L Butler, Bradley Ceely, Kathryn N North, David S Winlaw, Jonathan R Egan, Sandra T Cooper
AIMS: Mitsugumin-53 (MG53/TRIM72) is an E3-ubiquitin ligase that rapidly accumulates at sites of membrane injury and plays an important role in membrane repair of skeletal and cardiac muscle. MG53 has been implicated in cardiac ischaemia-reperfusion injury, and serum MG53 provides a biomarker of skeletal muscle injury in the mdx mouse model of Duchenne muscular dystrophy. We evaluated the clinical utility of MG53 as a biomarker of myocardial injury. METHODS AND RESULTS: We performed Langendorff ischaemia-reperfusion injury on wild-type and dysferlin-null murine hearts, using dysferlin deficiency to effectively model more severe outcomes from cardiac ischaemia-reperfusion injury...
May 15, 2016: Cardiovascular Research
Alexis R Demonbreun, Elizabeth M McNally
Since an intact membrane is required for normal cellular homeostasis, membrane repair is essential for cell survival. Human genetic studies, combined with the development of novel animal models and refinement of techniques to study cellular injury, have now uncovered series of repair proteins highly relevant for human health. Many of the deficient repair pathways manifest in skeletal muscle, where defective repair processes result in myopathies or other forms of muscle disease. Dysferlin is a membrane-associated protein implicated in sarcolemmal repair and also linked to other membrane functions including the maintenance of transverse tubules in muscle...
2016: Current Topics in Membranes
Haichang Li, Pu Duann, Pei-Hui Lin, Li Zhao, Zhaobo Fan, Tao Tan, Xinyu Zhou, Mingzhai Sun, Minghuan Fu, Matthew Orange, Matthew Sermersheim, Hanley Ma, Duofen He, Steven M Steinberg, Robert Higgins, Hua Zhu, Elizabeth John, Chunyu Zeng, Jianjun Guan, Jianjie Ma
Cell membrane repair is an important aspect of physiology, and disruption of this process can result in pathophysiology in a number of different tissues, including wound healing, chronic ulcer and scarring. We have previously identified a novel tripartite motif family protein, MG53, as an essential component of the cell membrane repair machinery. Here we report the functional role of MG53 in the modulation of wound healing and scarring. Although MG53 is absent from keratinocytes and fibroblasts, remarkable defects in skin architecture and collagen overproduction are observed in mg53(-/-) mice, and these animals display delayed wound healing and abnormal scarring...
October 2, 2015: Journal of Biological Chemistry
Hanley Ma, Jason Liu, Zehua Bian, Yuqi Cui, Xinyu Zhou, Xuefeng Zhou, Bo Zhang, T M Ayodele Adesanya, Frank Yi, Ki Ho Park, Tao Tan, Zhishui Chen, Hua Zhu
Metabolic syndrome is a cluster of risk factors, such as obesity, insulin resistance, and hyperlipidemia that increases the individual's likelihood of developing cardiovascular diseases. Patients inflicted with metabolic disorders also suffer from tissue repair defect. Mitsugumin 53 (MG53) is a protein essential to cellular membrane repair. It facilitates the nucleation of intracellular vesicles to sites of membrane disruption to create repair patches, contributing to the regenerative capacity of skeletal and cardiac muscle tissues upon injury...
2015: PloS One
Chuanxi Cai, Peihui Lin, Hua Zhu, Jae-Kyun Ko, Moonsun Hwang, Tao Tan, Zui Pan, Irina Korichneva, Jianjie Ma
Zinc is an essential trace element that participates in a wide range of biological functions, including wound healing. Although Zn(2+) deficiency has been linked to compromised wound healing and tissue repair in human diseases, the molecular mechanisms underlying Zn(2+)-mediated tissue repair remain unknown. Our previous studies established that MG53, a TRIM (tripartite motif) family protein, is an essential component of the cell membrane repair machinery. Domain homology analysis revealed that MG53 contains two Zn(2+)-binding motifs...
May 29, 2015: Journal of Biological Chemistry
Pu Duann, Haichang Li, Peihui Lin, Tao Tan, Zhen Wang, Ken Chen, Xinyu Zhou, Kristyn Gumpper, Hua Zhu, Thomas Ludwig, Peter J Mohler, Brad Rovin, William T Abraham, Chunyu Zeng, Jianjie Ma
Injury to the renal proximal tubular epithelium (PTE) represents the underlying consequence of acute kidney injury (AKI) after exposure to various stressors, including nephrotoxins and ischemia/reperfusion (I/R). Although the kidney has the ability to repair itself after mild injury, insufficient repair of PTE cells may trigger inflammatory and fibrotic responses, leading to chronic renal failure. We report that MG53, a member of the TRIM family of proteins, participates in repair of injured PTE cells and protects against the development of AKI...
March 18, 2015: Science Translational Medicine
Hua Zhu, Jincai Hou, Janet L Roe, Ki Ho Park, Tao Tan, Yongqiu Zheng, Lei Li, Cuixiang Zhang, Jianxun Liu, Zhenguo Liu, Jianjie Ma, Thomas J Walters
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...
November 2015: Muscle & Nerve
Jianxun Liu, Hua Zhu, Yongqiu Zheng, Zhaobin Xu, Lei Li, Tao Tan, Ki Ho Park, Jincai Hou, Cuixiang Zhang, Dan Li, Ran Li, Zhenguo Liu, Noah Weisleder, Desheng Zhu, Peihui Lin, Jianjie Ma
Ischemic heart disease is a leading cause of death in human population and protection of myocardial infarction (MI) associated with ischemia-reperfusion (I/R) remains a challenge. MG53 is an essential component of the cell membrane repair machinery that protects injury to the myocardium. We investigated the therapeutic value of using the recombinant human MG53 (rhMG53) protein for treatment of MI. Using Langendorff perfusion of isolated mouse heart, we found that I/R caused injury to cardiomyocytes and release of endogenous MG53 into the extracellular solution...
March 2015: Journal of Molecular and Cellular Cardiology
Xin Li, Yuan Xiao, Yuqi Cui, Tao Tan, Chandrakala A Narasimhulu, Hong Hao, Lingjuan Liu, Jia Zhang, Guanglong He, Catherine M Verfaillie, Minxiang Lei, Sampath Parthasarathy, Jianjie Ma, Hua Zhu, Zhenguo Liu
Cell therapy with bone marrow stem cells (BMSCs) remains a viable option for tissue repair and regeneration. A major challenge for cell therapy is the limited cell survival after implantation. This study was to investigate the effect of oxidized low-density lipoprotein (ox-LDL, naturally present in human blood) on BMSC injury and the effect of MG53, a tissue repair protein, for the improvement of stem cell survival. Rat bone marrow multipotent adult progenitor cells (MAPCs) were treated with ox-LDL, which caused significant cell death as reflected by the increased LDH release to the media...
December 2014: Journal of Cellular and Molecular Medicine
Sandra Palus, Stephan von Haehling, Jochen Springer
The syndrome of cachexia, i.e. involuntary weight loss in patients with underlying diseases, sarcopenia, i.e. loss of muscle mass due to ageing, and general muscle atrophy from disuse and/or prolonged bed rest have received more attention over the last decades. All lead to a higher morbidity and mortality in patients and therefore, they represent a major socio-economic burden for the society today. This mini-review looks at recent developments in basic research that are relevant to the loss of skeletal muscle...
October 20, 2014: International Journal of Cardiology
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