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muscle protein degradation

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https://www.readbyqxmd.com/read/27928928/effects-of-mushroom-extract-on-textural-properties-and-muscle-protein-degradation-of-bovine-longissimus-dorsi-muscle
#1
Kyung-Ha Lee, Ho-Kyoung Kim, Sae-Hun Kim, Kyoung-Hwan Kim, Young-Min Choi, Hyun-Hee Jin, Seung-Joo Lee, Youn-Chul Ryu
We investigated the effects of Sarcodon aspratus, Agaricus bisporus, and Lentinula edodes aqueous extracts on the tenderization of bovine longissimus dorsi muscle. Meat quality and muscle protein degradation were examined as well. Beef chunks were marinated in distilled water (control), 5% S. aspratus (SA), 5% A. bisporus (AB), or 5% L. edodes (LE) extracts. SA was shown to have a higher enzymatic activity (p < 0.001) and water-holding capacity than LE (p < 0.01). SA and AB extracts exhibited lower shear force values compared with the control (p < 0...
December 8, 2016: Bioscience, Biotechnology, and Biochemistry
https://www.readbyqxmd.com/read/27922672/2-methoxycinnamaldehyde-inhibits-the-tnf-%C3%AE-induced-proliferation-and-migration-of-human-aortic-smooth-muscle-cells
#2
Young-Hee Jin, Soo-A Kim
The abnormal proliferation and migration of vascular smooth muscle cells (VSMCs) is a crucial event in the development of atherosclerosis, and tumor necrosis factor-α (TNF-α) is actively involved in this process by enhancing the proliferation and migration of VSMCs. 2-Methoxycinnamaldehyde (MCA) is a natural compound of Cinnamomum cassia. Although 2-hydroxycinnamaldehyde (HCA), another compound from Cinnamomum cassia, has been widely studied with regard to its antitumor activity, MCA has not attracted researchers' interest due to its mild toxic effects on cancer cells and its mechanisms of action remain unknown...
December 6, 2016: International Journal of Molecular Medicine
https://www.readbyqxmd.com/read/27906069/the-beneficial-role-of-proteolysis-in-skeletal-muscle-growth-and-stress-adaptation
#3
REVIEW
Ryan A V Bell, Mohammad Al-Khalaf, Lynn A Megeney
Muscle atrophy derived from excessive proteolysis is a hallmark of numerous disease conditions. Accordingly, the negative consequences of skeletal muscle protein breakdown often overshadow the critical nature of proteolytic systems in maintaining normal cellular function. Here, we discuss the major cellular proteolysis machinery-the ubiquitin/proteosome system, the autophagy/lysosomal system, and caspase-mediated protein cleavage-and the critical role of these protein machines in establishing and preserving muscle health...
April 6, 2016: Skeletal Muscle
https://www.readbyqxmd.com/read/27904835/a-novel-dominant-d109a-cryab-mutation-in-a-family-with-myofibrillar-myopathy-affects-%C3%AE-b-crystallin-structure
#4
Jakub P Fichna, Anna Potulska-Chromik, Przemysław Miszta, Maria Jolanta Redowicz, Anna M Kaminska, Cezary Zekanowski, Sławomir Filipek
Myofibrillar myopathy (MFM) is a group of inherited muscular disorders characterized by myofibrils dissolution and abnormal accumulation of degradation products. So far causative mutations have been identified in nine genes encoding Z-disk proteins, including αB-crystallin (CRYAB), a small heat shock protein (also called HSPB5). Here, we report a case study of a 63-year-old Polish female with a progressive lower limb weakness and muscle biopsy suggesting a myofibrillar myopathy, and extra-muscular multisystemic involvement, including cataract and cardiomiopathy...
June 2017: BBA Clinical
https://www.readbyqxmd.com/read/27897418/suppression-of-muscle-wasting-by-the-plant-derived-compound-ursolic-acid-in-a-model-of-chronic-kidney-disease
#5
Rizhen Yu, Ji-An Chen, Jing Xu, Jin Cao, Yanlin Wang, Sandhya S Thomas, Zhaoyong Hu
BACKGROUND: Muscle wasting in chronic kidney disease (CKD) and other catabolic disorders contributes to morbidity and mortality, and there are no therapeutic interventions that regularly and safely block losses of muscle mass. We have obtained evidence that impaired IGF-1/insulin signalling and increases in glucocorticoids, myostatin and/or inflammatory cytokines that contribute to the development of muscle wasting in catabolic disorders by activating protein degradation. METHODS: Using in vitro and in vivo models of muscle wasting associated with CKD or dexamethasone administration, we measured protein synthesis and degradation and examined mechanisms by which ursolic acid, derived from plants, could block the loss of muscle mass stimulated by CKD or excessive levels of dexamethasone...
November 17, 2016: Journal of Cachexia, Sarcopenia and Muscle
https://www.readbyqxmd.com/read/27897407/activin-a-induces-skeletal-muscle-catabolism-via-p38%C3%AE-mitogen-activated-protein-kinase
#6
Hui Ding, Guohua Zhang, Ka Wai Thomas Sin, Zhelong Liu, Ren-Kuo Lin, Min Li, Yi-Ping Li
BACKGROUND: Activation of type IIB activin receptor (ActRIIB) in skeletal muscle leads to muscle atrophy because of increased muscle protein degradation. However, the intracellular signalling mechanism that mediates ActRIIB-activated muscle catabolism is poorly defined. METHODS: We investigated the role of p38β mitogen-activated protein kinases (MAPK) in mediating ActRIIB ligand activin A-activated muscle catabolic pathways in C2C12 myotubes and in mice with perturbation of this kinase pharmacologically and genetically...
September 16, 2016: Journal of Cachexia, Sarcopenia and Muscle
https://www.readbyqxmd.com/read/27893734/an-ipsc-derived-vascular-model-of-marfan-syndrome-identifies-key-mediators-of-smooth-muscle-cell-death
#7
Alessandra Granata, Felipe Serrano, William George Bernard, Madeline McNamara, Lucinda Low, Priya Sastry, Sanjay Sinha
Marfan syndrome (MFS) is a heritable connective tissue disorder caused by mutations in FBN1, which encodes the extracellular matrix protein fibrillin-1. To investigate the pathogenesis of aortic aneurysms in MFS, we generated a vascular model derived from human induced pluripotent stem cells (MFS-hiPSCs). Our MFS-hiPSC-derived smooth muscle cells (SMCs) recapitulated the pathology seen in Marfan aortas, including defects in fibrillin-1 accumulation, extracellular matrix degradation, transforming growth factor-β (TGF-β) signaling, contraction and apoptosis; abnormalities were corrected by CRISPR-based editing of the FBN1 mutation...
November 28, 2016: Nature Genetics
https://www.readbyqxmd.com/read/27889204/tauroursodeoxycholic-acid-attenuates-angiotensin-ii-induced-abdominal-aortic-aneurysm-formation-in-apolipoprotein-e-deficient-mice-by-inhibiting-endoplasmic-reticulum-stress
#8
Y Qin, Y Wang, O Liu, L Jia, W Fang, J Du, Y Wei
OBJECTIVE/BACKGROUND: Abdominal aortic aneurysm (AAA) is characterised by the infiltration of smooth muscle cell (SMC) apoptosis, inflammatory cells, neovascularisation, and degradation of the extracellular matrix. Previous work has shown that endoplasmic reticulum (ER) stress and SMC apoptosis were increased both in a mouse model and human thoracic aortic aneurysm. However, whether the ER stress is activated in AAA formation and whether suppressing ER stress attenuates AAA is unknown...
November 24, 2016: European Journal of Vascular and Endovascular Surgery
https://www.readbyqxmd.com/read/27882347/ml372-blocks-smn-ubiquitination-and-improves-spinal-muscular-atrophy-pathology-in-mice
#9
Mahlet B Abera, Jingbo Xiao, Jonathan Nofziger, Steve Titus, Noel Southall, Wei Zheng, Kasey E Moritz, Marc Ferrer, Jonathan J Cherry, Elliot J Androphy, Amy Wang, Xin Xu, Christopher Austin, Kenneth H Fischbeck, Juan J Marugan, Barrington G Burnett
Spinal muscular atrophy (SMA) is an autosomal recessive neuromuscular disease and one of the leading inherited causes of infant mortality. SMA results from insufficient levels of the survival motor neuron (SMN) protein, and studies in animal models of the disease have shown that increasing SMN protein levels ameliorates the disease phenotype. Our group previously identified and optimized a new series of small molecules, with good potency and toxicity profiles and reasonable pharmacokinetics, that were able to increase SMN protein levels in SMA patient-derived cells...
November 17, 2016: JCI Insight
https://www.readbyqxmd.com/read/27880894/requirement-for-dicer-in-maintenance-of-monosynaptic-sensory-motor-circuits-in-the-spinal-cord
#10
Fumiyasu Imai, Xiaoting Chen, Matthew T Weirauch, Yutaka Yoshida
In contrast to our knowledge of mechanisms governing circuit formation, our understanding of how neural circuits are maintained is limited. Here, we show that Dicer, an RNaseIII protein required for processing microRNAs (miRNAs), is essential for maintenance of the spinal monosynaptic stretch reflex circuit in which group Ia proprioceptive sensory neurons form direct connections with motor neurons. In postnatal mice lacking Dicer in proprioceptor sensory neurons, there are no obvious defects in specificity or formation of monosynaptic sensory-motor connections...
November 22, 2016: Cell Reports
https://www.readbyqxmd.com/read/27880847/activation-of-both-the-calpain-and-ubiquitin-proteasome-systems-contributes-to-septic-cardiomyopathy-through-dystrophin-loss-disruption-and-mtor-inhibition
#11
Ana Caroline Silva Freitas, Maria Jose Figueiredo, Erica Carolina Campos, Danilo Figueiredo Soave, Simone Gusmao Ramos, Herbert B Tanowitz, Mara Rúbia N Celes
Cardiac dysfunction caused by the impairment of myocardial contractility has been recognized as an important factor contributing to the high mortality in sepsis. Calpain activation in the heart takes place in response to increased intracellular calcium influx resulting in proteolysis of structural and contractile proteins with subsequent myocardial dysfunction. The purpose of the present study was to test the hypothesis that increased levels of calpain in the septic heart leads to disruption of structural and contractile proteins and that administration of calpain inhibitor-1 (N-acetyl-leucinyl-leucinyl-norleucinal (ALLN)) after sepsis induced by cecal ligation and puncture prevents cardiac protein degradation...
2016: PloS One
https://www.readbyqxmd.com/read/27875962/the-beneficial-effects-of-taurine-to-counteract-sarcopenia
#12
Bianca M Scicchitano, Gigliola Sica
Aging is a multifactorial process characterized by several features including low-grade inflammation, increased oxidative stress and reduced regenerative capacity, which ultimately lead to alteration in morpho-functional properties of skeletal muscle, thus promoting sarcopenia. This condition is characterized by a gradual loss of muscle mass due to an unbalance between protein synthesis and degradation, finally conveying in functional decline and disability. The development of specific therapeutic approaches able to block or reverse this condition may represent an invaluable tool for the promotion of a healthy aging among elderly...
November 22, 2016: Current Protein & Peptide Science
https://www.readbyqxmd.com/read/27875947/skeletal-muscle-insulin-resistance-as-a-precursor-to-diabetes-beyond-glucoregulation
#13
Nicholas P Greene, Jacob L Brown, Megan E Rosa-Caldwell, David E Lee, Thomas A Blackwell, Tyrone A Washington
Prevalence of Type 2 Diabetes Mellitus (T2DM) has reached pandemic levels in Western societies. T2DM begins with the development of peripheral insulin resistance which prior research suggests may commonly originate within skeletal muscle. A number of mechanisms have been proposed for the development of muscle insulin resistance including those of classical glucose handling, but also other cellular derangements observed in this disease which include mitochondrial degeneration, alterations in muscle protein turnover and early evidences for dysregulation of microRNAs...
November 22, 2016: Current Diabetes Reviews
https://www.readbyqxmd.com/read/27875560/denervation-induced-activation-of-the-standard-proteasome-and-immunoproteasome
#14
Haiming M Liu, Deborah A Ferrington, Cory W Baumann, LaDora V Thompson
The standard 26S proteasome is responsible for the majority of myofibrillar protein degradation leading to muscle atrophy. The immunoproteasome is an inducible form of the proteasome. While its function has been linked to conditions of atrophy, its contribution to muscle proteolysis remains unclear. Therefore, the purpose of this study was to determine if the immunoproteasome plays a role in skeletal muscle atrophy induced by denervation. Adult male C57BL/6 wild type (WT) and immunoproteasome knockout lmp7-/-/mecl-1-/- (L7M1) mice underwent tibial nerve transection on the left hindlimb for either 7 or 14 days, while control mice did not undergo surgery...
2016: PloS One
https://www.readbyqxmd.com/read/27874066/cl316-243-a-%C3%AE-3-adrenergic-receptor-agonist-induces-muscle-hypertrophy-and-increased-strength
#15
Daniela Puzzo, Roberto Raiteri, Clotilde Castaldo, Raffaele Capasso, Ester Pagano, Mariateresa Tedesco, Walter Gulisano, Lisaveta Drozd, Pellegrino Lippiello, Agostino Palmeri, Pietro Scotto, Maria Concetta Miniaci
Studies in vitro have demonstrated that β3-adrenergic receptors (β3-ARs) regulate protein metabolism in skeletal muscle by promoting protein synthesis and inhibiting protein degradation. In this study, we evaluated whether activation of β3-ARs by the selective agonist CL316,243 modifies the functional and structural properties of skeletal muscles of healthy mice. Daily injections of CL316,243 for 15 days resulted in a significant improvement in muscle force production, assessed by grip strength and weight tests, and an increased myofiber cross-sectional area, indicative of muscle hypertrophy...
November 22, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27870901/ubiquitin-dependent-modification-of-skeletal-muscle-by-the-parasitic-nematode-trichinella-spiralis
#16
Rhiannon R White, Amy H Ponsford, Michael P Weekes, Rachel B Rodrigues, David B Ascher, Marco Mol, Murray E Selkirk, Steven P Gygi, Christopher M Sanderson, Katerina Artavanis-Tsakonas
Trichinella spiralis is a muscle-specific parasitic worm that is uniquely intracellular. T. spiralis reprograms terminally differentiated skeletal muscle cells causing them to de-differentiate and re-enter the cell cycle, a process that cannot occur naturally in mammalian skeletal muscle cells, but one that holds great therapeutic potential. Although the host ubiquitin pathway is a common target for viruses and bacteria during infection, its role in parasite pathogenesis has been largely overlooked. Here we demonstrate that the secreted proteins of T...
November 2016: PLoS Pathogens
https://www.readbyqxmd.com/read/27866730/hereditary-neuropathies-an-update
#17
REVIEW
T Stojkovic
Hereditary neuropathies are the most common inherited neuromuscular diseases. Charcot-Marie-Tooth (CMT) disease represents the most common form with an average prevalence ranging from 1/2500 to 1/1200, depending on the studies. To date and with the advances of the latest generation sequencing, more than 80 genes have been identified. Although the common clinical phenotype comprises a progressive distal muscle weakness and sensory loss, foot deformities and decreased or absent tendon reflexes, clinical and electrophysiological phenotypes exhibit great variability...
December 2016: Revue Neurologique
https://www.readbyqxmd.com/read/27863213/tubular-cytoplasmic-expression-of-snai1-in-renal-transplant-biopsies-a-sign-of-diseased-epithelial-phenotype
#18
Marco Prunotto, Lyubov Chaykovska, Massimo Bongiovanni, Milo Frattini, Thomas Cagarelli, Franziska Weibel, Maurizio Bruschi, Antonio Garcia de Herreros, Solange Moll
The aim of the present study was to analyze in vivo the role of SNAI1 on renal fibrosis. Unilateral ureteral obstruction injury was induced in Snai1 knockout mice. Snai1 gene deletion was, however, only partial and could therefore not be correlated to reduced fibrosis. Expression of SNAI1 protein and epithelial-mesenchymal transformation markers was then assessed in human chronic allograft nephropathy biopsy specimens. Significant up-regulation of SNAI1 protein was detected within cytoplasm of proximal tubules localized, for some of them, near foci of fibrosis and tubular atrophy...
November 15, 2016: American Journal of Pathology
https://www.readbyqxmd.com/read/27854226/neo-epitope-peptides-as-biomarkers-of-disease-progression-for-muscular-dystrophies-and-other-myopathies
#19
A Arvanitidis, K Henriksen, M A Karsdal, A Nedergaard
For several decades, serological biomarkers of neuromuscular diseases as dystrophies, myopathies and myositis have been limited to routine clinical biochemistry panels. Gauging the pathological progression is a prerequisite for proper treatment and therefore identifying accessible, easy to monitor biomarkers that can predict the disease progression would be an important advancement. Most muscle diseases involve accelerated muscle fiber degradation, inflammation, fatty tissue substitution and/or fibrosis. All these pathological traits have been shown to give rise to serological peptide biomarkers in other tissues, underlining the potential application of existing biomarkers of such traits in muscle disorders...
August 30, 2016: Journal of Neuromuscular Diseases
https://www.readbyqxmd.com/read/27845200/a-combination-of-korean-mistletoe-extract-and-resistance-exercise-retarded-the-decline-in-muscle-mass-and-strength-in-the-elderly-a-randomized-controlled-trial
#20
Nam Ju Lim, Jun Ho Shin, Hye Jin Kim, Yeni Lim, Ji Yeon Kim, Won Jun Lee, Soo Jeong Han, Oran Kwon
Given the increased concerns about the degenerative decline in the physical performance of the elderly, there is a need for developing effective strategies to suppress the age-related loss of skeletal muscle mass and functional capacity through a lifestyle intervention. This randomized controlled trial examined whether a combination of Korean mistletoe extract (KME) supplement and exercise affected muscle mass, muscle function, and targeted molecular expressions. Sixty-seven subjects aged 55-75years were assigned to placebo, low-dose (1g/d), or high-dose (2g/d) of KME for 12weeks...
November 11, 2016: Experimental Gerontology
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