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https://www.readbyqxmd.com/read/27843952/swimming-exercise-alleviated-insulin-resistance-by-regulating-tripartite-motif-family-protein-72-expression-and-akt-signal-pathway-in-sprague-dawley-rats-fed-with-high-fat-diet
#1
Jie Qi, Bo Yang, Cailing Ren, Jian Fu, Jun Zhang
We aimed to investigate whether swimming exercise could improve insulin resistance (IR) by regulating tripartite motif family protein 72 (TRIM72) expression and AKT signal pathway in rats fed with high-fat diet. Five-week-old rats were classified into 3 groups: standard diet as control (CON), high-fat diet (HFD), and HFD plus swimming exercise (Ex-HFD). After 8 weeks, glucose infusion rate (GIR), markers of oxidative stress, mRNA and protein expression of TRIM72, protein of IRS, p-AKT(Ser473), and AKT were determined in quadriceps muscles...
2016: Journal of Diabetes Research
https://www.readbyqxmd.com/read/27546510/mg53-is-a-double-edged-sword-for-human-diseases
#2
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]
https://www.readbyqxmd.com/read/26985866/tripartite-motif-protein-72-regulates-the-proliferation-and-migration-of-rat-cardiac-fibroblasts-via-the-transforming-growth-factor-%C3%AE-signaling-pathway
#3
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
https://www.readbyqxmd.com/read/26790476/lack-of-mg53-in-human-heart-precludes-utility-as-a-biomarker-of-myocardial-injury-or-endogenous-cardioprotective-factor
#4
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
https://www.readbyqxmd.com/read/26637632/trim72-modulates-caveolar-endocytosis-in-repair-of-lung-cells
#5
Nagaraja Nagre, Shaohua Wang, Thomas Kellett, Ragu Kanagasabai, Jing Deng, Miyuki Nishi, Konstantin Shilo, Richard A Oeckler, Jack C Yalowich, Hiroshi Takeshima, John Christman, Rolf D Hubmayr, Xiaoli Zhao
Alveolar epithelial and endothelial cell injury is a major feature of the acute respiratory distress syndrome, in particular when in conjunction with ventilation therapies. Previously we showed [Kim SC, Kellett T, Wang S, Nishi M, Nagre N, Zhou B, Flodby P, Shilo K, Ghadiali SN, Takeshima H, Hubmayr RD, Zhao X. Am J Physiol Lung Cell Mol Physiol 307: L449-L459, 2014.] that tripartite motif protein 72 (TRIM72) is essential for amending alveolar epithelial cell injury. Here, we posit that TRIM72 improves cellular integrity through its interaction with caveolin 1 (Cav1)...
March 1, 2016: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/25830844/modulation-of-trim72-alters-the-repair-capacity-of-lung-epithelial-cells
#6
Seong Chul Kim, Thomas Kellett, Shaohua Wang, Miyuki Nishi, Nagaraja Nagre, Beiyun Zhou, Per Flodby, Konstantin Shilo, Samir N Ghadiali, Hiroshi Takeshima, Rolf D Hubmayr, Xiaoli Zhao
No abstract text is available yet for this article.
March 2015: Annals of the American Thoracic Society
https://www.readbyqxmd.com/read/25701873/the-e3-ubiquitin-ligase-trim32-regulates-myoblast-proliferation-by-controlling-turnover-of-ndrg2
#7
Ekaterina I Mokhonova, Nuraly K Avliyakulov, Irina Kramerova, Elena Kudryashova, Michael J Haykinson, Melissa J Spencer
Limb girdle muscular dystrophy 2H is caused by mutations in the gene encoding the E3 ubiquitin ligase, TRIM32. Previously, we generated and characterized a Trim32 knockout mouse (T32KO) that displays both neurogenic and myopathic features. The myopathy in these mice is attributable to impaired muscle growth, associated with satellite cell senescence and premature sarcopenia. This satellite cell senescence is due to accumulation of the SUMO ligase PIASy, a substrate of TRIM32. The goal of this investigation was to identify additional substrates of TRIM32 using 2D fluorescence difference gel electrophoresis (2D-DIGE) in order to further explore its role in skeletal muscle...
May 15, 2015: Human Molecular Genetics
https://www.readbyqxmd.com/read/25539835/loading-associated-expression-of-trim72-and-caveolin-3-in-antigravitational-soleus-muscle-in-mice
#8
Yoshitaka Ohno, Takao Sugiura, Yoshinobu Ohira, Toshitada Yoshioka, Katsumasa Goto
Effects of mechanical loading on the expression level of tripartite motif-containing 72 (TRIM72) and caveolin-3 (Cav-3) in mouse soleus muscle were investigated. Mice were subjected to (1) continuous hindlimb suspension (HS) for 2 weeks followed by 1-week ambulation recovery or (2) functional overloading (FO) on the soleus by cutting the distal tendons of the plantaris and gastrocnemius muscles. Soleus muscle atrophy was induced by 2-week hindlimb suspension (HS). Reloading-associated regrowth of atrophied soleus muscle was observed by 1-week reloading following HS...
December 1, 2014: Physiological Reports
https://www.readbyqxmd.com/read/25205489/muscle-wasting-an-overview-of-recent-developments-in-basic-research
#9
REVIEW
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
https://www.readbyqxmd.com/read/25163459/muscle-wasting-an-overview-of-recent-developments-in-basic-research
#10
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 aging, 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...
September 2014: Journal of Cachexia, Sarcopenia and Muscle
https://www.readbyqxmd.com/read/25106429/trim72-is-required-for-effective-repair-of-alveolar-epithelial-cell-wounding
#11
Seong Chul Kim, Thomas Kellett, Shaohua Wang, Miyuki Nishi, Nagaraja Nagre, Beiyun Zhou, Per Flodby, Konstantin Shilo, Samir N Ghadiali, Hiroshi Takeshima, Rolf D Hubmayr, Xiaoli Zhao
The molecular mechanisms for lung cell repair are largely unknown. Previous studies identified tripartite motif protein 72 (TRIM72) from striated muscle and linked its function to tissue repair. In this study, we characterized TRIM72 expression in lung tissues and investigated the role of TRIM72 in repair of alveolar epithelial cells. In vivo injury of lung cells was introduced by high tidal volume ventilation, and repair-defective cells were labeled with postinjury administration of propidium iodide. Primary alveolar epithelial cells were isolated and membrane wounding and repair were labeled separately...
September 15, 2014: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/24772964/expression-levels-of-sarcolemmal-membrane-repair-proteins-following-prolonged-exercise-training-in-mice
#12
Jenna Alloush, Steve R Roof, Eric X Beck, Mark T Ziolo, Noah Weisleder
Membrane repair is a conserved cellular process, where intracellular vesicles translocate to sites of plasma membrane injury to actively reseal membrane disruptions. Such membrane disruptions commonly occur in the course of normal physiology, particularly in skeletal muscles due to repeated contraction producing small tears in the sarcolemmal membrane. Here, we investigated whether prolonged exercise could produce adaptive changes in expression levels of proteins associated with the membrane repair process, including mitsugumin 53/tripartite motif-containing protein 72 (MG53/TRIM72), dysferlin and caveolin-3 (cav3)...
October 2013: Indian Journal of Biochemistry & Biophysics
https://www.readbyqxmd.com/read/24735828/s-nitrosylation-of-trim72-mends-the-broken-heart-a-molecular-modifier-mediated-cardioprotection
#13
EDITORIAL
C Y X'avia Chan, Ding Wang, Martin Cadeiras, Mario C Deng, Peipei Ping
No abstract text is available yet for this article.
July 2014: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/24487118/s-nitrosylation-of-trim72-at-cysteine-144-is-critical-for-protection-against-oxidation-induced-protein-degradation-and-cell-death
#14
Mark J Kohr, Alicia M Evangelista, Marcella Ferlito, Charles Steenbergen, Elizabeth Murphy
Oxidative stress and membrane damage following myocardial ischemia/reperfusion injury are important contributors to cardiomyocyte death and the loss of myocardial function. Our previous study identified cysteine 144 (C144) of tripartite motif-containing protein 72 (TRIM72) as a potential site for S-nitrosylation (SNO). TRIM72 is a cardioprotective membrane repair protein that can be both activated and targeted for degradation by different oxidative modifications. Consistent with the potential regulation of TRIM72 by various oxidative modifications, we found that SNO levels increased at C144 of TRIM72 with ischemic preconditioning...
April 2014: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/24401845/proteomic-mapping-of-proteins-released-during-necrosis-and-apoptosis-from-cultured-neonatal-cardiac-myocytes
#15
COMPARATIVE STUDY
Kurt D Marshall, Michelle A Edwards, Maike Krenz, J Wade Davis, Christopher P Baines
Cardiac injury induces myocyte apoptosis and necrosis, resulting in the secretion and/or release of intracellular proteins. Currently, myocardial injury can be detected by analysis of a limited number of biomarkers in blood or coronary artery perfusate. However, the complete proteomic signature of protein release from necrotic cardiac myocytes is unknown. Therefore, we undertook a proteomic-based study of proteins released from cultured neonatal rat cardiac myocytes in response to H2O2 (necrosis) or staurosporine (apoptosis) to identify novel specific markers of cardiac myocyte cell death...
April 1, 2014: American Journal of Physiology. Cell Physiology
https://www.readbyqxmd.com/read/23792176/dysferlin-interacts-with-calsequestrin-1-myomesin-2-and-dynein-in-human-skeletal-muscle
#16
Bàrbara Flix, Carolina de la Torre, Juan Castillo, Carme Casal, Isabel Illa, Eduard Gallardo
Dysferlinopathies are a group of progressive muscular dystrophies characterized by mutations in the gene DYSF. These mutations cause scarcity or complete absence of dysferlin, a protein that is expressed in skeletal muscle and plays a role in membrane repair. Our objective was to unravel the proteins that constitute the dysferlin complex and their interaction within the complex using immunoprecipitation assays (IP), blue native gel electrophoresis (BN) in healthy adult skeletal muscle and healthy cultured myotubes, and fluorescence lifetime imaging-fluorescence resonance energy transfer (FLIM-FRET) analysis in healthy myotubes...
August 2013: International Journal of Biochemistry & Cell Biology
https://www.readbyqxmd.com/read/23699904/trim-proteins-in-therapeutic-membrane-repair-of-muscular-dystrophy
#17
REVIEW
Jenna Alloush, Noah Weisleder
Muscular dystrophy represents a major unmet medical need; only palliative treatments exist for this group of debilitating diseases. Because multiple forms of muscular dystrophy arise from compromised sarcolemmal membrane integrity, a therapeutic approach that can target this loss of membrane function could be applicable to a number of these distinct diseases.One promising therapeutic approach involves the process the cell uses to repair injuries to the plasma membrane. Recent discoveries of genes associated with the membrane repair process provide an opportunity to promote this process as a way to treat muscular dystrophy...
July 2013: JAMA Neurology
https://www.readbyqxmd.com/read/23567182/compensation-of-the-akt-signaling-by-erk-signaling-in-transgenic-mice-hearts-overexpressing-trim72
#18
Young-Mi Ham, Sarah Jane Mahoney
The AKT and ERK signaling pathways are known to be involved in cell hypertrophy, proliferation, survival and differentiation. Although there is evidence for crosstalk between these two signaling pathways in cellulo, there is less evidence for cross talk in vivo. Here, we show that crosstalk between AKT and ERK signaling in the hearts of TRIM72-overexpressing transgenic mice (TRIM72-Tg) with alpha-MHC promoter regulates and maintains their heart size. TRIM72, a heart- and skeletal muscle-specific protein, downregulates AKT-mTOR signaling via IRS-1 degradation and reduces the size of rat cardiomyocytes and the size of postnatal TRIM72-Tg hearts...
June 10, 2013: Experimental Cell Research
https://www.readbyqxmd.com/read/23354051/central-role-of-e3-ubiquitin-ligase-mg53-in-insulin-resistance-and-metabolic-disorders
#19
Ruisheng Song, Wei Peng, Yan Zhang, Fengxiang Lv, Hong-Kun Wu, Jiaojiao Guo, Yongxing Cao, Yanbin Pi, Xin Zhang, Li Jin, Mao Zhang, Peng Jiang, Fenghua Liu, Shaoshuai Meng, Xiuqin Zhang, Ping Jiang, Chun-Mei Cao, Rui-Ping Xiao
Insulin resistance is a fundamental pathogenic factor present in various metabolic disorders including obesity and type 2 diabetes. Although skeletal muscle accounts for 70-90% of insulin-stimulated glucose disposal, the mechanism underlying muscle insulin resistance is poorly understood. Here we show in mice that muscle-specific mitsugumin 53 (MG53; also called TRIM72) mediates the degradation of the insulin receptor and insulin receptor substrate 1 (IRS1), and when upregulated, causes metabolic syndrome featuring insulin resistance, obesity, hypertension and dyslipidaemia...
February 21, 2013: Nature
https://www.readbyqxmd.com/read/23145354/the-c2a-domain-in-dysferlin-is-important-for-association-with-mg53-trim72
#20
Chie Matsuda, Katsuya Miyake, Kimihiko Kameyama, Etsuko Keduka, Hiroshi Takeshima, Toru Imamura, Nobukazu Araki, Ichizo Nishino, Yukiko Hayashi
In skeletal muscle, Mitsugumin 53 (MG53), also known as muscle-specific tripartite motif 72, reportedly interacts with dysferlin to regulate membrane repair. To better understand the interactions between dysferlin and MG53, we conducted immunoprecipitation (IP) and pull-down assays. Based on IP assays, the C2A domain in dysferlin associated with MG53. MG53 reportedly exists as a monomer, a homodimer, or an oligomer, depending on the redox state. Based on pull-down assays, wild-type dysferlin associated with MG53 dimers in a Ca2+-dependent manner, but MG53 oligomers associated with both wild-type and C2A-mutant dysferlin in a Ca2+-independent manner...
2012: PLoS Currents
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