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https://www.readbyqxmd.com/read/28104914/docosahexaenoic-acid-mediated-protein-aggregates-may-reduce-proteasome-activity-and-delay-myotube-degradation-during-muscle-atrophy-in-vitro
#1
Seung Kyun Shin, Ji Hyeon Kim, Jung Hoon Lee, Young Hoon Son, Min Wook Lee, Hak Joong Kim, Sue Ah Noh, Kwang Pyo Kim, In-Gyu Kim, Min Jae Lee
Proteasomes are the primary degradation machinery for oxidatively damaged proteins that compose a class of misfolded protein substrates. Cellular levels of reactive oxygen species increase with age and this cellular propensity is particularly harmful when combined with the age-associated development of various human disorders including cancer, neurodegenerative disease and muscle atrophy. Proteasome activity is reportedly downregulated in these disease conditions. Herein, we report that docosahexaenoic acid (DHA), a major dietary omega-3 polyunsaturated fatty acid, mediates intermolecular protein cross-linkages through oxidation, and the resulting protein aggregates potently reduce proteasomal activity both in vitro and in cultured cells...
January 20, 2017: Experimental & Molecular Medicine
https://www.readbyqxmd.com/read/28104751/exercise-training-decreases-nadph-oxidase-activity-and-restores-skeletal-muscle-mass-in-heart-failure-rats
#2
Telma F Cunha, Luiz Roberto Grassman Bechara, Aline V N Bacurau, Paulo R Jannig, Vanessa Azevedo Voltarelli, Paulo M Dourado, Andrea R Vasconcelos, Cristóforo Scavone, Julio C B Ferreira, Patricia C Brum
We have recently demonstrated that NADPH oxidase hyperactivity, NF-κB activation and increased p38 phosphorylation lead to atrophy of glycolytic muscle in heart failure (HF). Aerobic exercise training (AET) is an efficient strategy to counteract skeletal muscle atrophy in this syndrome. Therefore, we tested whether AET would regulate muscle redox balance and protein degradation by decreasing NADPH oxidase hyperactivity, reestablishing NF-κB signaling, p38 phosphorylation and proteasome activity in plantaris muscle of myocardial infarcted-induced HF (MI) rats...
January 19, 2017: Journal of Applied Physiology
https://www.readbyqxmd.com/read/28101649/molecular-mechanism-of-sarcopenia-and-cachexia-recent-research-advances
#3
REVIEW
Kunihiro Sakuma, Wataru Aoi, Akihiko Yamaguchi
Skeletal muscle provides a fundamental basis for human function, enabling locomotion and respiration. Muscle loss occurs as a consequence of several chronic diseases (cachexia) and normal aging (sarcopenia). Although many negative regulators (atrogin-1, muscle ring finger-1, nuclear factor-kappaB (NF-κB), myostatin, etc.) have been proposed to enhance protein degradation during both sarcopenia and cachexia, the adaptation of these mediators markedly differs within both conditions. Sarcopenia and cachectic muscles have been demonstrated to be abundant in myostatin-linked molecules...
January 19, 2017: Pflügers Archiv: European Journal of Physiology
https://www.readbyqxmd.com/read/28097232/vps34-regulates-myofibril-proteostasis-to-prevent-hypertrophic-cardiomyopathy
#4
Hirotaka Kimura, Satoshi Eguchi, Junko Sasaki, Keiji Kuba, Hiroki Nakanishi, Shunsuke Takasuga, Masakazu Yamazaki, Akiteru Goto, Hiroyuki Watanabe, Hiroshi Itoh, Yumiko Imai, Akira Suzuki, Noboru Mizushima, Takehiko Sasaki
Hypertrophic cardiomyopathy (HCM) is a common heart disease with a prevalence of 1 in 500 in the general population. Several mutations in genes encoding cardiac proteins have been found in HCM patients, but these changes do not predict occurrence or prognosis and the molecular mechanisms underlying HCM remain largely elusive. Here we show that cardiac expression of vacuolar protein sorting 34 (Vps34) is reduced in a subset of HCM patients. In a mouse model, muscle-specific loss of Vps34 led to HCM-like manifestations and sudden death...
January 12, 2017: JCI Insight
https://www.readbyqxmd.com/read/28096335/myofibril-breakdown-during-atrophy-is-a-delayed-response-requiring-the-transcription-factor-pax4-and-desmin-depolymerization
#5
Alexandra Volodin, Idit Kosti, Alfred Lewis Goldberg, Shenhav Cohen
A hallmark of muscle atrophy is the excessive degradation of myofibrillar proteins primarily by the ubiquitin proteasome system. In mice, during the rapid muscle atrophy induced by fasting, the desmin cytoskeleton and the attached Z-band-bound thin filaments are degraded after ubiquitination by the ubiquitin ligase tripartite motif-containing protein 32 (Trim32). To study the order of events leading to myofibril destruction, we investigated the slower atrophy induced by denervation (disuse). We show that myofibril breakdown is a two-phase process involving the initial disassembly of desmin filaments by Trim32, which leads to the later myofibril breakdown by enzymes, whose expression is increased by the paired box 4 (PAX4) transcription factor...
January 17, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/28094956/radiolabeled-r954-derivatives-for-imaging-bradykinin-b1-receptor-expression-with-positron-emission-tomography
#6
Hsiou-Ting Kuo, Jinhe Pan, Joseph Lau, Chengcheng Zhang, Jutta Zeisler, Nadine Colpo, Francois Benard, Kuo-Shyan Lin
Peptide receptors have emerged as promising targets for diagnosis and therapy. The aberrant overexpression of these receptors in different cancer subtypes allows for the adoption of new treatment strategies that complement conventional chemotherapies. Bradykinin B1 receptor (B1R) is a G protein-coupled receptor that is overexpressed in many cancers, with limited expression in healthy tissues. Previously, we developed 68Ga- and 18F-labeled derivatives of B1R antagonist peptides B9858 and B9958, and successfully targeted B1R-expressing tumor xenografts in vivo...
January 17, 2017: Molecular Pharmaceutics
https://www.readbyqxmd.com/read/28077463/novel-method-for-detection-of-glycogen-in-cells
#7
Alexander V Skurat, Dyann Segvich, Anna A DePaoli-Roach, Peter J Roach
Glycogen, a branched polymer of glucose, functions as an energy reserve in many living organisms. Abnormalities in glycogen metabolism, usually excessive accumulation, can be caused genetically, most often through mutation of the enzymes directly involved in synthesis and degradation of the polymer leading to a variety of glycogen storage diseases (GSDs). Microscopic visualization of glycogen deposits in cells and tissues is important for the study of normal glycogen metabolism as well as diagnosis of GSDs...
January 10, 2017: Glycobiology
https://www.readbyqxmd.com/read/28067271/praja1-e3-ubiquitin-ligase-promotes-skeletal-myogenesis-through-degradation-of-ezh2-upon-p38%C3%AE-activation
#8
Silvia Consalvi, Arianna Brancaccio, Alessandra Dall'Agnese, Pier Lorenzo Puri, Daniela Palacios
Polycomb proteins are critical chromatin modifiers that regulate stem cell differentiation via transcriptional repression. In skeletal muscle progenitors Enhancer of zeste homologue 2 (EZH2), the catalytic subunit of Polycomb Repressive Complex 2 (PRC2), contributes to maintain the chromatin of muscle genes in a repressive conformation, whereas its down-regulation allows the progression through the myogenic programme. Here, we show that p38α kinase promotes EZH2 degradation in differentiating muscle cells through phosphorylation of threonine 372...
January 9, 2017: Nature Communications
https://www.readbyqxmd.com/read/28062506/wnt-signaling-pathway-inhibitor-sclerostin-inhibits-angiotensin-ii-induced-aortic-aneurysm-and-atherosclerosis
#9
Smriti Murali Krishna, Sai-Wang Seto, Roby J Jose, Jiaze Li, Susan K Morton, Erik Biros, Yutang Wang, Vianne Nsengiyumva, Jan H N Lindeman, Gabriela G Loots, Catherine M Rush, Jeffrey M Craig, Jonathan Golledge
OBJECTIVE: Sclerostin (SOST) has been identified as an important regulator of bone formation; however, it has not been previously implicated in arterial disease. The aim of this study was to assess the role of SOST in aortic aneurysm (AA) and atherosclerosis using human samples, a mouse model, and in vitro investigations. APPROACH AND RESULTS: SOST protein was downregulated in human and mouse AA samples compared with controls. Transgenic introduction of human SOST in apolipoprotein E-deficient (ApoE(-/-)) mice (SOST(Tg)...
December 22, 2016: Arteriosclerosis, Thrombosis, and Vascular Biology
https://www.readbyqxmd.com/read/28040730/mutations-in-the-accessory-subunit-ndufb10-result-in-isolated-complex-i-deficiency-and-illustrate-the-critical-role-of-intermembrane-space-import-for-complex-i-holoenzyme-assembly
#10
Marisa W Friederich, Alican J Erdogan, Curtis R Coughlin, Mihret T Elos, Hua Jiang, Courtney O'Rourke, Mark A Lovell, Eric Wartchow, Katherine Gowan, Kathryn C Chatfield, Wallace S Chick, Elaine Spector, Johan L K Van Hove, Jan Riemer
An infant presented with fatal infantile lactic acidosis and cardiomyopathy, and was found to have profoundly decreased activity of respiratory chain complex I in muscle, heart and liver. Exome sequencing revealed compound heterozygous mutations in NDUFB10, an accessory subunit located within the PD part of complex I. One mutation resulted in a premature stop codon and absent protein, while the second mutation replaced the highly conserved cysteine 107 with a serine residue. Protein expression of NDUFB10 was decreased in muscle and heart, and less so in liver and fibroblasts, resulting in perturbed assembly of the holoenzyme at the 830 kDa stage...
December 30, 2016: Human Molecular Genetics
https://www.readbyqxmd.com/read/28039193/short-term-intense-exercise-training-reduces-stress-markers-and-alters-the-transcriptional-response-to-exercise-in-skeletal-muscle
#11
James Matthew Hinkley, Adam R Konopka, Miranda K Suer, Matthew P Harber
The purpose of this investigation was to examine the influence of short-term intense endurance training on cycling performance, along with the acute and chronic signaling responses of skeletal muscle stress and stability markers. Ten recreationally active subjects (25 ± 2 yr, 79 ± 3 kg, 47 ± 2 ml·kg·min-1) were studied before and after a 12-day cycling protocol to examine the effects of short-term intense (70-100% VO2max) exercise training on resting and exercise-induced regulation of molecular factors related to skeletal muscle cellular stress and protein stability...
December 30, 2016: American Journal of Physiology. Regulatory, Integrative and Comparative Physiology
https://www.readbyqxmd.com/read/28036018/effects-of-supplementation-of-branched-chain-amino-acids-to-reduced-protein-diet-on-skeletal-muscle-protein-synthesis-and-degradation-in-the-fed-and-fasted-states-in-a-piglet-model
#12
Liufeng Zheng, Hongkui Wei, Pingli He, Shengjun Zhao, Quanhang Xiang, Jiaman Pang, Jian Peng
Supplementation of branched-chain amino acids (BCAA) has been demonstrated to promote skeletal muscle mass gain, but the mechanisms underlying this observation are still unknown. Since the regulation of muscle mass depends on a dynamic equilibrium (fasted losses-fed gains) in protein turnover, the aim of this study was to investigate the effects of BCAA supplementation on muscle protein synthesis and degradation in fed/fasted states and the related mechanisms. Fourteen 26- (Experiment 1) and 28-day-old (Experiment 2) piglets were fed reduced-protein diets without or with supplemental BCAA...
December 28, 2016: Nutrients
https://www.readbyqxmd.com/read/28018906/chaperonopathies-spotlight-on-hereditary-motor-neuropathies
#13
REVIEW
Vincenzo Lupo, Carmen Aguado, Erwin Knecht, Carmen Espinós
Distal hereditary motor neuropathies (dHMN) are a group of rare hereditary neuromuscular disorders characterized by an atrophy that affects peroneal muscles in the absence of sensory symptoms. To date, 23 genes are thought to be responsible for dHMN, four of which encode chaperones: DNAJB2, which encodes a member of the HSP40/DNAJ co-chaperone family; and HSPB1, HSPB3, and HSPB8, encoding three members of the small heat shock protein family. While around 30 different mutations in HSPB1 have been identified, the remaining three genes are altered in many fewer cases...
2016: Frontiers in Molecular Biosciences
https://www.readbyqxmd.com/read/28011640/regulation-of-ulk1-expression-and-autophagy-by-stat1
#14
Alexander A Goldberg, Bernard Nkengfac, Anthony M J Sanchez, Nikolay Moroz, Salman T Qureshi, Antonis E Koromilas, Shuo Wang, Yan Burelle, Sabah N Hussain, Arnold S Kristof
Autophagy involves the lysosomal degradation of cytoplasmic contents for regeneration of anabolic substrates during nutritional or inflammatory stress. Its initiation occurs rapidly after inactivation of the protein- kinase 'mammalian target of rapamycin' (mTOR; or 'mechanistic target of rapamycin', MTOR), leading to de-phosphorylation of Unc-51-like kinase 1 (ULK1) and autophagosome formation. Recent studies indicate that mTOR can, in parallel, regulate the activity of stress transcription factors, including 'signal transducer and activator of transcription-1' (STAT1)...
December 23, 2016: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/28009790/exercise-training-reverses-extrapulmonary-impairments-in-smoke-exposed-mice
#15
T Scott Bowen, Lars Aakerøy, Sophia Eisenkolb, Patricia Kunth, Fredrik Bakkerud, Martin Wohlwend, Anne Marie Ormbostad, Tina Fischer, Ulrik Wisloff, Gerhard Schuler, Sigurd Steinshamn, Volker Adams, Eivind Bronstad
PURPOSE: Cigarette smoking is the main risk factor for chronic obstructive pulmonary disease and emphysema. However, evidence on the extrapulmonary effects of smoke exposure that precede lung impairments remains unclear at present, as are data on non-pharmacological treatments such as exercise training. METHODS: Three groups of mice including control (n=10), smoking (n=10), and smoking with 6 weeks of high-intensity interval treadmill running (n=11) were exposed to 20 weeks of fresh air or whole-body cigarette smoke...
December 22, 2016: Medicine and Science in Sports and Exercise
https://www.readbyqxmd.com/read/28009536/leucine-protects-against-skeletal-muscle-atrophy-in-lipopolysaccharide-challenged-rats
#16
Jin Wan, Daiwen Chen, Bing Yu, Yuheng Luo, Xiangbing Mao, Ping Zheng, Jie Yu, Junqiu Luo, Jun He
Skeletal muscle atrophy is a decrease in muscle mass that occurs when protein degradation exceeds protein synthesis. Leucine (Leu), an essential branched-chain amino acid in animal nutrition, regulates skeletal muscle protein metabolism. Two experiments were conducted to evaluate whether Leu could alleviate lipopolysaccharide (LPS)-induced skeletal muscle wasting by modulating skeletal muscle protein synthesis and degradation. A total of 24 rats were randomly allocated into three groups (n = 8): (1) non-challenged control; (2) LPS-challenged control; and (3) LPS +3...
January 2017: Journal of Medicinal Food
https://www.readbyqxmd.com/read/28009083/proteomics-of-rimmed-vacuoles-define-new-risk-allele-in-inclusion-body-myositis
#17
Anne-Katrin Güttsches, Stefen Brady, Kathryn Krause, Alexandra Maerkens, Julian Uszkoreit, Martin Eisenacher, Anja Schreiner, Sara Galozzi, Janine Mertens-Rill, Martin Tegenthoff, Janice L Holton, Matthew B Harms, Thomas E Lloyd, Matthias Vorgerd, Conrad C Weihl, Katrin Marcus, Rudolf A Kley
OBJECTIVE: Sporadic inclusion body myositis (sIBM) pathogenesis is unknown; however, rimmed vacuoles (RVs) are a constant feature. We propose to identify proteins that accumulate within RVs. METHODS: RVs and intact myofibers were laser microdissected from skeletal muscle of 18 sIBM patients and analyzed by a sensitive mass spectrometry approach using label-free spectral count-based relative protein quantification. Whole exome sequencing was performed on 62 sIBM patients...
December 23, 2016: Annals of Neurology
https://www.readbyqxmd.com/read/28002075/what-factors-influence-protein-synthesis-and-degradation-in-critical-illness
#18
Filippo G Di Girolamo, Roberta Situlin, Gianni Biolo
PURPOSE OF REVIEW: The optimal approach to improve protein metabolism in critical illness is not yet fully defined. Here, we have summarized recent literature dealing with the main catabolic and anabolic factors influencing protein kinetics in acute hypercatabolic patients. RECENT FINDINGS: Protein/amino acid intake levels should be adapted to type and severity of illness, keeping in mind that energy overfeeding is associated with poor outcome. A number of anticatabolic nutraceuticals and drugs have been tested in acute patients...
December 20, 2016: Current Opinion in Clinical Nutrition and Metabolic Care
https://www.readbyqxmd.com/read/28000044/dysregulation-between-trim63-fbxo32-expression-and-soleus-muscle-wasting-in-diabetic-rats-potential-role-of-mir-1-3p-29a-b-3p-and-133a-b-3p
#19
Frederico Gerlinger-Romero, Caio Yogi Yonamine, Danilo Correa Pinto Junior, João Victor DelConti Esteves, Ubiratan Fabres Machado
Diabetes mellitus (DM) induces a variable degree of muscle sarcopenia, which may be related to protein degradation and to the expression of both E3 ubiquitin ligases and some specific microRNAs (miRNAs). The present study investigated the effect of diabetes and acute muscle contraction upon the TRIM63 and FBXO32 expression as well as the potential involvement of some miRNAs. Diabetes was induced by streptozotocin and studied after 30 days. Soleus muscles were harvested, stimulated to contract in vitro for twitch tension analysis (0...
December 20, 2016: Molecular and Cellular Biochemistry
https://www.readbyqxmd.com/read/27993671/effect-of-acute-and-chronic-autophagy-deficiency-on-skeletal-muscle-apoptotic-signaling-morphology-and-function
#20
M F Paré, B L Baechler, V A Fajardo, E Earl, E Wong, T L Campbell, A R Tupling, J Quadrilatero
Autophagy is a catabolic process that targets and degrades cytoplasmic materials. In skeletal muscle, autophagy is required for the control of mass under catabolic conditions, but is also basally active in the maintenance of myofiber homeostasis. In this study, we found that some specific autophagic markers (LC3-I, LC3-II, SQSTM1) were basally lower in glycolytic muscle compared to oxidative muscle of autophagy competent mice. In contrast, basal autophagic flux was higher in glycolytic muscle. In addition, we used several skeletal muscle-specific Atg7 transgenic mouse models to investigate the effect of acute (iAtg7(-/-)) and chronic (cAtg7(-/-)) autophagy deficiency on skeletal muscle morphology, contractility, and apoptotic signaling...
December 16, 2016: Biochimica et Biophysica Acta
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