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(Muscle Protein) AND (Degradation or breakdown or atrophy or loss)

Kenyu Hayashi, Yu Hasegawa, Yushin Takemoto, Cheng Cao, Hiroto Takeya, Yoshihiro Komohara, Akitake Mukasa, Shokei Kim-Mitsuyama
Systemic organ dysfunction is one of the important issues for the patients with Alzheimer's disease (AD) and their caregivers. Recent evidences suggest that periodontitis is a possible risk factor for progression of AD and lipopolysaccharide derived from Porphyromonas gingivalis (Pg-LPS) which is a major periodontopathic bacteria induces cognitive impairment in mice. However, the precise relationships between the brain exposure of Pg-LPS and systemic organ dysfunction in AD patients are still undetermined. In this study, we investigated whether brain exposure of Pg-LPS induced systemic organ dysfunction in a model of AD mouse...
February 17, 2019: Experimental Gerontology
Jordan J S VerPlank, Sudarsanareddy Lokireddy, Jinghui Zhao, Alfred L Goldberg
Pharmacological agents that raise cAMP and activate protein kinase A (PKA) stimulate 26S proteasome activity, phosphorylation of subunit Rpn6, and intracellular degradation of misfolded proteins. We investigated whether a similar proteasome activation occurs in response to hormones and under various physiological conditions that raise cAMP. Treatment of mouse hepatocytes with glucagon, epinephrine, or forskolin stimulated Rpn6 phosphorylation and the 26S proteasomes' capacity to degrade ubiquitinated proteins and peptides...
February 19, 2019: Proceedings of the National Academy of Sciences of the United States of America
Yash Chhabra, Caroline N Nelson, Monika Plescher, Johanna L Barclay, Aaron G Smith, Sof Andrikopoulos, Salvatore Mangiafico, David J Waxman, Andrew J Brooks, Michael J Waters
Growth hormone (GH) has an important function as an insulin antagonist with elevated insulin sensitivity evident in humans and mice lacking a functional GH receptor (GHR). We sought the molecular basis for this sensitivity by utilizing a panel of mice possessing specific deletions of GHR signaling pathways. Metabolic clamps and glucose homeostasis tests were undertaken in these obese adult C57BL/6 male mice, which indicated impaired hepatic gluconeogenesis. Insulin sensitivity and glucose disappearance rate were enhanced in muscle and adipose of mice lacking the ability to activate the signal transducer and activator of transcription (STAT)5 via the GHR ( Ghr-391 -/- ) as for GHR-null ( GHR-/- ) mice...
February 19, 2019: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
Marion Mussbacher, Manuel Salzmann, Christine Brostjan, Bastian Hoesel, Christian Schoergenhofer, Hannes Datler, Philipp Hohensinner, José Basílio, Peter Petzelbauer, Alice Assinger, Johannes A Schmid
The transcription factor NF-κB is a central mediator of inflammation with multiple links to thrombotic processes. In this review, we focus on the role of NF-κB signaling in cell types within the vasculature and the circulation that are involved in thrombo-inflammatory processes. All these cells express NF-κB, which mediates important functions in cellular interactions, cell survival and differentiation, as well as expression of cytokines, chemokines, and coagulation factors. Even platelets, as anucleated cells, contain NF-κB family members and their corresponding signaling molecules, which are involved in platelet activation, as well as secondary feedback circuits...
2019: Frontiers in Immunology
Sathnur Pushpakumar, Sourav Kundu, Utpal Sen
The accumulation of homocysteine (Hcy) during chronic kidney failure (CKD) can exert toxic effects on the glomeruli and tubulo-interstitial region. Among the potential mechanisms, the formation of highly reactive metabolite, Hcy thiolactone, is known to modify proteins by N-homocysteinylation, leading to protein degradation, stress and impaired function. Previous studies documented impaired nitric oxide production and altered caveolin expression in hyperhomocysteinemia (HHcy), leading to endothelial dysfunction...
February 18, 2019: Scientific Reports
Yasukiyo Yoshioka, Yusuke Kubota, Yumi Samukawa, Yoko Yamashita, Hitoshi Ashida
Prevention of muscle wasting is known to contribute to improving the quality of life and extending a healthy life. Recently, we have reported that licorice flavonoid oil containing glabridin, which is a prenylated isoflavone, enhances muscle mass in mice. In this study, we investigated the prevention effect of glabridin on dexamethasone-induced muscle atrophy and clarified its mechanism in cultured myotubes and in muscle of mice. Treatment with glabridin to C2C12 myotubes inhibited dexamethasone-induced protein degradation through dexamethasone-induced expression of ubiquitin ligases, MuRF1 and Cbl-b, but not atrogin-1...
February 13, 2019: Archives of Biochemistry and Biophysics
Heikkinen Anne, Härönen Heli, Norman Oula, Pihlajaniemi Taina
Alongside playing structural roles, the extracellular matrix (ECM) acts as an interaction platform for cellular homeostasis, organ development, and maintenance. The necessity of the ECM is highlighted by the diverse, sometimes very serious diseases that stem from defects in its components. The neuromuscular junction (NMJ) is a large peripheral motor synapse differing from its central counterparts through the ECM included at the synaptic cleft. Such synaptic basal lamina (BL) is specialized to support NMJ establishment, differentiation, maturation, stabilization, and function and diverges in molecular composition from the extrasynaptic ECM...
February 15, 2019: Anatomical Record: Advances in Integrative Anatomy and Evolutionary Biology
Harold W Lee, Ella Baker, Kevin M Lee, Aaron Michael Persinger, William Hawkins, Melissa Puppa
Many forms of cancer are associated with loss of lean body mass, commonly attributed to decreased protein synthesis and stimulation of proteolytic pathways within the skeletal muscle. Leucine has been shown to improve protein synthesis, insulin signaling, and mitochondrial biogenesis, key signaling pathways influenced by tumor signaling. The purpose of this study was to examine the effects of leucine supplementation on mitochondrial biogenesis and protein turnover in tumor bearing mice. Twenty male C57BL/6 mice were divided into four groups (n=5): Chow, leucine (Leu), Lewis lung carcinoma (LLC) implant, LLC+Leu...
February 15, 2019: Applied Physiology, Nutrition, and Metabolism, Physiologie Appliquée, Nutrition et Métabolisme
Zhihuan Tian, Chuanzhen Jiao
BACKGROUND: Molting is a critical developmental process for crustaceans, during which the claw muscles undergo periodic atrophy and restoration. But the mechanism underlying this special muscle reshuffle around ecdysis is not yet thoroughly understood. OBJECTIVE: To investigate the molecular mechanism underlying the muscle's reshuffle over the molting cycle of Chinese mitten crab Eriocheir sinensis. METHODS: The Illumina high-throughput sequencing technique were used to sequence the transcriptome of the whole claw muscles from Chinese mitten crab Eriocheir sinensis in three molting stages (inter-molt C stage, pre-molt D3-4 and post-molt A-B stage); the de novo assembly, annotation and functional evaluation of the contigs were performed with bioinformatics tools...
February 14, 2019: Genes & Genomics
Evgenii Bogatikov, Ida Lindblad, Tanel Punga, Anna Rostedt Punga
MuSK antibody seropositive (MuSK+) Myasthenia Gravis (MG) typically affects skeletal muscles of the bulbar area, including the omohyoid muscle, causing focal fatigue, weakness and atrophy. The profile of circulating extracellular microRNA (miRNA) is changed in MuSK + MG, but the intracellular miRNA profile in skeletal muscles of MuSK + MG and MuSK + experimental autoimmune MG (EAMG) remains unknown. This study elucidated the intracellular miRNA profile in the omohyoid muscle of mice with MuSK + EAMG...
February 11, 2019: Neuroscience Research
Andrea Palermo, Lorenzo Sanesi, Graziana Colaianni, Gaia Tabacco, Anda Mihaela Naciu, Roberto Cesareo, Claudio Pedone, Diana Lelli, Giacomina Brunetti, Giorgio Mori, Silvia Colucci, Silvia Manfrini, Nicola Napoli, Maria Grano
Context: Irisin is a hormone like-molecule that is cleaved and secreted by an unknown protease from fibronectin type III domain-containing protein 5 (FNDC5) and it ameliorates bone status, muscle atrophy and influences energy homeostasis. PTH exerts several metabolic effects that may interact with irisin's ones. Objectives: To test the hypothesis that irisin and PTH mutually affect their biological action, we evaluated the FNDC5 mRNA and protein expression in myotubes treated with PTH (1-34) and PTH-r mRNA expression in osteoblasts treated with rec-irisin...
February 13, 2019: Journal of Clinical Endocrinology and Metabolism
Takahiro Yajima, Maiko Arao, Kumiko Yajima, Hiroshi Takahashi, Keigo Yasuda
Protein-energy wasting, which involves loss of fat and muscle mass, is prevalent and is associated with mortality in hemodialysis (HD) patients. We investigated the associations of fat tissue and muscle mass indices with all-cause mortality in HD patients. The study included 162 patients undergoing HD. The fat tissue index (FTI) and skeletal muscle mass index (SMI), which represent respective tissue masses normalized to height squared, were measured by bioimpedance analysis after dialysis. Patients were divided into the following four groups according to the medians of FTI and SMI values: group 1 (G1), lower FTI and lower SMI; G2, higher FTI and lower SMI; G3, lower FTI and higher SMI; and G4, higher FTI and higher SMI...
2019: PloS One
Ashley N Haddock, Sydney A Labuzan, Amy E Haynes, Caleb S Hayes, Karina M Kakareka, David S Waddell
Skeletal muscle atrophy results from disparate physiological conditions, including denervation, corticosteroid treatment, and aging. The purpose of this study was to describe and characterize the function of dual-specificity phosphatase 4 (Dusp4) in skeletal muscle after it was found to be induced in response to neurogenic atrophy. qPCR and Western blot analysis revealed that Dusp4 is expressed during myoblast proliferation, but rapidly disappears as muscle cells differentiate. The Dusp4 regulatory region was cloned and found to contain a conserved E-box element that negatively regulates Dusp4 reporter gene activity in response to myogenic regulatory factor expression...
February 13, 2019: American Journal of Physiology. Cell Physiology
Xueting Gao, Siyun Gao, Yi Guan, Lin Huang, Jiale Huang, Li Lin, Yuan Liu, Hong Zhao, Bijun Huang, Tianyou Yuan, Yi Liu, Dandan Liang, Yangyang Zhang, Xiue Ma, Li Li, Jun Li, Daizhan Zhou, Dan Shi, Liang Xu, Yi-Han Chen
TLRs have been proven to be essential mediators for the early innate immune response. Overactivation of TLR-mediated immune signaling promotes deterioration of cardiovascular diseases; however, the role of TLRs in the heart under physiologic conditions remains neglected. Here, we show that Tlr3 deficiency induced the endoplasmic reticulum (ER) retention of Kv4.2/4.3 proteins and consequent degradation via the ubiquitin-proteasome pathway. Knockout of Tlr3 resulted in a prolonged QT interval (the space between the start of the Q wave and the end of the T wave) in mice with no significant signs of inflammation and tissue abnormality in cardiac muscles...
February 13, 2019: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
Yu Kitaoka, Yuki Tamura, Kenya Takahashi, Kohei Takeda, Tohru Takemasa, Hideo Hatta
Oxidative stress and mitochondrial dysfunction are associated with the aging process. However, the role of nuclear factor erythroid 2 -related factor 2 (Nrf2) in skeletal muscle during aging remains to be clarified. In the current study, we assessed whether the lack of Nrf2, which is known as a master regulator of redox homeostasis, promotes age-related mitochondrial dysfunction and muscle atrophy in skeletal muscle. Here, we demonstrated that mitochondrial 4-hydroxynonenal and protein carbonyls, markers of oxidative stress, were robustly elevated in aged Nrf2 knockout (KO) mice because of the decreased expression of Nrf2-target antioxidant genes...
February 2019: Physiological Reports
Lina Antounians, Areti Tzanetakis, Ornella Pellerito, Vincenzo D Catania, Adrienne Sulistyo, Louise Montalva, Mark J McVey, Augusto Zani
Extracellular vesicles (EVs) derived from amniotic fluid stem cells (AFSCs) mediate anti-apoptotic, pro-angiogenic, and immune-modulatory effects in multiple disease models, such as skeletal muscle atrophy and Alport syndrome. A source of potential variability in EV biological functions is how EV are isolated from parent cells. Currently, a comparative study of different EV isolation strategies using conditioned medium from AFSCs is lacking. Herein, we examined different isolation strategies for AFSC-EVs, using common techniques based on differential sedimentation (ultracentrifugation), solubility (ExoQuick, Total Exosome Isolation Reagent, Exo-PREP), or size-exclusion chromatography (qEV)...
February 12, 2019: Scientific Reports
K J Hughes, A Rodriguez, K M Flatt, S Ray, A Schuler, B Rodemoyer, V Veerappan, K Cuciarone, A Kullman, C Lim, N Gutta, S Vemuri, V Andriulis, D Niswonger, L Barickman, W Stein, A Singhvi, N E Schroeder, A G Vidal-Gadea
Duchenne muscular dystrophy (DMD) is a genetic disorder caused by loss of the protein dystrophin. In humans, DMD has early onset, causes developmental delays, muscle necrosis, loss of ambulation, and death. Current animal models have been challenged by their inability to model the early onset and severity of the disease. It remains unresolved whether increased sarcoplasmic calcium observed in dystrophic muscles follows or leads the mechanical insults caused by the muscle's disrupted contractile machinery. This knowledge has important implications for patients, as potential physiotherapeutic treatments may either help or exacerbate symptoms, depending on how dystrophic muscles differ from healthy ones...
February 12, 2019: Proceedings of the National Academy of Sciences of the United States of America
Muhannad Abu-Remaileh, Monther Abu-Remaileh, Rania Akkawi, Ibrahim Knani, Shiran Udi, Micheal E Pacold, Joseph Tam, Rami I Aqeilan
OBJECTIVE: WWOX, a well-established tumor suppressor, is frequently lost in cancer and plays important roles in DNA damage response and cellular metabolism. METHODS: We re-analyzed several genome-wide association studies (GWAS) using the Type 2 Diabetes Knowledge Portal website to uncover WWOX's association with metabolic syndrome (MetS). Using several engineered mouse models, we studied the effect of somatic WWOX loss on glucose homeostasis. RESULTS: Several WWOX variants were found to be strongly associated with MetS disorders...
January 31, 2019: Molecular Metabolism
N E H Dinesh, D P Reinhardt
Mutations in extracellular matrix and smooth muscle cell contractile proteins predispose to thoracic aortic aneurysms in Marfan syndrome (MFS) and related disorders. These genetic alterations lead to a compromised extracellular matrix-smooth muscle cell contractile unit. The abnormal aortic tissue responds with defective mechanosensing under hemodynamic stress. Aberrant mechanosensing is associated with transforming growth factor-beta (TGF-β) hyperactivity, enhanced angiotensin-II (Ang-II) signaling, and perturbation of other cellular signaling pathways...
February 12, 2019: Herz
Mizuho Ishikawa, Mitsuhiko Osaki, Makoto Yamagishi, Kunishige Onuma, Hisao Ito, Futoshi Okada, Hideya Endo
Extensive studies on metastasis-associated proteins, S100A4 and MTA1, have been carried out for over two decades, but correlation of both proteins remains obscure. Here we show evidence for the correlation in angiogenesis. First, silencing of each protein by siRNA-mediated knockdown in mouse endothelial MSS31 cells resulted in the inhibition of tube formation. Unexpectedly, the knockdown of MTA1 affected not only its own expression but also the expression of S100A4, whereas silencing of S100A4 did not affect the MTA1 expression...
February 11, 2019: Oncogene
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