Zinc Binding to MG53 Protein Facilitates Repair of Injury to Cell Membranes

Cai, Chuanxi; Lin, Pei‐Hui; Zhu, Hua; Ko, Jae‐Woong; Hwang, Moonsun; Tan, Tao; Pan, Zui; Korichneva, Irina; Ma, Jianjie

doi:10.1074/jbc.m114.620690

Cited by 36 publications

(34 citation statements)

References 54 publications

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“…Disruption of membrane integrity or impaired membrane repair could result in pathological changes including cell death in a variety of organ systems and cells . Recent studies have identified some proteins that are critically involved in membrane repair and maintaining the membrane integrity for cell survival and optimal cell function . MG53 is a muscle‐specific tripartite motif (TRIM) family protein with 477 amino acids and is an essential component of the acute membrane repair machinery .…”

Section: Discussionmentioning

confidence: 99%

N‐acetylcysteine prevents oxidized low‐density lipoprotein‐induced reduction of MG53 and enhances MG53 protective effect on bone marrow stem cells

Jiang

Tan

et al. 2019

J Cellular Molecular Medi

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MG53 is an important membrane repair protein and partially protects bone marrow multipotent adult progenitor cells (MAPCs) against oxidized low‐density lipoprotein (ox‐LDL). The present study was to test the hypothesis that the limited protective effect of MG53 on MAPCs was due to ox‐LDL‐induced reduction of MG53. MAPCs were cultured with and without ox‐LDL (0‐20 μg/mL) for up to 48 hours with or without MG53 and antioxidant N‐acetylcysteine (NAC). Serum MG53 level was measured in ox‐LDL‐treated mice with or without NAC treatment. Ox‐LDL induced significant membrane damage and substantially impaired MAPC survival with selective inhibition of Akt phosphorylation. NAC treatment effectively prevented ox‐LDL‐induced reduction of Akt phosphorylation without protecting MAPCs against ox‐LDL. While having no effect on Akt phosphorylation, MG53 significantly decreased ox‐LDL‐induced membrane damage and partially improved the survival, proliferation and apoptosis of MAPCs in vitro. Ox‐LDL significantly decreased MG53 level in vitro and serum MG53 level in vivo without changing MG53 clearance. NAC treatment prevented ox‐LDL‐induced MG53 reduction both in vitro and in vivo. Combined NAC and MG53 treatment significantly improved MAPC survival against ox‐LDL. These data suggested that NAC enhanced the protective effect of MG53 on MAPCs against ox‐LDL through preventing ox‐LDL‐induced reduction of MG53.

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Section: Discussionmentioning

confidence: 99%

N‐acetylcysteine prevents oxidized low‐density lipoprotein‐induced reduction of MG53 and enhances MG53 protective effect on bone marrow stem cells

Jiang

Tan

et al. 2019

J Cellular Molecular Medi

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“…It was observed that recombinant TRIM72 tends to polymerize through its cysteine residues under native condition (102), and Snitrosylation of TRIM72 at cysteine-144 was shown to be important for protection of cardiomyocytes from oxidative insults (129,279). Other studies also reported that nonmuscle myosin type IIA served as a motor to translocate TRIM72 during repair (149), and Zn 2ϩ binding to TRIM72 was important for its repair function (30). Furthermore, cholesterol content in the plasma membrane was shown to greatly affect injury-induced membrane translocation of TRIM72 and cell repair in ischemia-reperfusion injury (271).…”

Section: Repair Mechanisms For Injured Lung Cellsmentioning

confidence: 99%

Plasma membrane wounding and repair in pulmonary diseases

Cong

Hubmayr

et al. 2017

American Journal of Physiology-Lung Cellular and Molecular Phys

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Various pathophysiological conditions such as surfactant dysfunction, mechanical ventilation, inflammation, pathogen products, environmental exposures, and gastric acid aspiration stress lung cells, and the compromise of plasma membranes occurs as a result. The mechanisms necessary for cells to repair plasma membrane defects have been extensively investigated in the last two decades, and some of these key repair mechanisms are also shown to occur following lung cell injury. Because it was theorized that lung wounding and repair are involved in the pathogenesis of acute respiratory distress syndrome (ARDS) and idiopathic pulmonary fibrosis (IPF), in this review, we summarized the experimental evidence of lung cell injury in these two devastating syndromes and discuss relevant genetic, physical, and biological injury mechanisms, as well as mechanisms used by lung cells for cell survival and membrane repair. Finally, we discuss relevant signaling pathways that may be activated by chronic or repeated lung cell injury as an extension of our cell injury and repair focus in this review. We hope that a holistic view of injurious stimuli relevant for ARDS and IPF could lead to updated experimental models. In addition, parallel discussion of membrane repair mechanisms in lung cells and injury-activated signaling pathways would encourage research to bridge gaps in current knowledge. Indeed, deep understanding of lung cell wounding and repair, and discovery of relevant repair moieties for lung cells, should inspire the development of new therapies that are likely preventive and broadly effective for targeting injurious pulmonary diseases.

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“…It is involved in iron transport and transfer [29,30,31] and enhances the immune system [32,33,34]. Zn can inhibit lipid peroxidation and thiol oxidation of biomembranes, and along with copper-protein, catalase, and vitamin E, maintains cell structure [35,36,37,38]. Zn deficiency causes digestive disorders, delayed sexual maturity/development of secondary sexual characteristics resulting in stunted growth, skin disease, stomatitis, alopecia [29,30,39], and can impair immune function.…”

Section: Introductionmentioning

confidence: 99%

Analysis of Blood Concentrations of Zinc, Germanium, and Lead and Relevant Environmental Factors in a Population Sample from Shandong Province, China

Xu²,

Shao³

et al. 2017

IJERPH

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Trace elements, including zinc (Zn) and germanium (Ge), are essential for health; deficiency or excess levels of trace elements results is harmful. As a result of industrial and agricultural production, Pb widely exists in people’s living environment. It is absorbed mainly through the respiratory and digestive tracts, producing systemic harm. Reference values for a normal, healthy population are necessary for health assessment, prevention and treatment of related diseases, and evaluation of occupational exposures. Reference ranges for the Chinese population have not been established. From March 2009 to February 2010; we collected data and blood samples (n = 1302) from residents aged 6–60 years living in Shandong Province, China. We measured blood concentrations of Zn, Ge, and Pb using inductively coupled plasma mass spectrometry to determine reference ranges. Results were stratified by factors likely to affect the concentrations of these trace elements: sex, use of cosmetics or hair dye, age, alcohol intake, smoking habits, and consumption of fried food. The overall geometric mean (GM) concentrations (95% confidence interval) were 3.14 (3.08–3.20) mg/L for Zn, 19.9 (19.3–20.6) μg/L for Ge, and 24.1 (23.2–25.1) μg/L for Pb. Blood Zn concentrations were higher in women than in men (p < 0.001), while the opposite was found for Pb (p < 0.001) and sex did not influence Ge (p = 0.095). Alcohol use was associated with higher blood concentrations of Zn (p = 0.002), Ge (p = 0.002), and Pb (p = 0.001). The GM concentration of Zn was highest in 20–30-year-olds (p < 0.001), while Pb concentrations were highest in 12–16-year-olds (p < 0.001). Use of hair dye was associated with lower blood concentrations of Ge (p < 0.05). GM blood concentrations of Pb differed significantly between those who consumed fried foods 1–2 times/month (18.7 μg/L), 1–2 times/week (20.9 μg/L), and every day (28.5 μg/L; p < 0.001). Blood Pb concentrations were higher in subjects who used cosmetics (p < 0.05), hair dye (p < 0.05), and who smoked cigarettes (p < 0.001) than in those who did not.

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Zinc Binding to MG53 Protein Facilitates Repair of Injury to Cell Membranes

Cited by 36 publications

References 54 publications

N‐acetylcysteine prevents oxidized low‐density lipoprotein‐induced reduction of MG53 and enhances MG53 protective effect on bone marrow stem cells

N‐acetylcysteine prevents oxidized low‐density lipoprotein‐induced reduction of MG53 and enhances MG53 protective effect on bone marrow stem cells

Plasma membrane wounding and repair in pulmonary diseases

Analysis of Blood Concentrations of Zinc, Germanium, and Lead and Relevant Environmental Factors in a Population Sample from Shandong Province, China

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