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Beclin 1 mitophagy

Sailaja Ghanta, Konstantin Tsoyi, Xiaoli Liu, Kiichi Nakahira, Bonna Ith, Anna A Coronata, Laura E Fredenburgh, Joshua A Englert, Claude A Piantadosi, Augustine M K Choi, Mark A Perrella
Oxidative stress resulting from inflammatory responses that occur during acute lung injury and sepsis can initiate changes in mitochondrial function. Autophagy regulates cellular processes in the setting of acute lung injury, sepsis, and oxidative stress by modulating the immune response and facilitating turnover of damaged cellular components. We have shown that mesenchymal stromal cells (MSCs) improve survival in murine models of sepsis by also regulating the immune response. However, the effect of autophagy on MSC and MSC mitochondrial function during oxidative stress is unknown...
September 16, 2016: American Journal of Respiratory Cell and Molecular Biology
I M Aparicio, J Espino, I Bejarano, A Gallardo-Soler, M L Campo, G M Salido, J A Pariente, F J Peña, J A Tapia
Macroautophagy (hereafter autophagy) is an evolutionarily highly conserved cellular process that participates in the maintenance of intracellular homeostasis through the degradation of most long-lived proteins and entire organelles. Autophagy participates in some reproductive events; however, there are not reports regarding the role of autophagy in the regulation of sperm physiology. Hence, the aim of this study was to investigate whether autophagy-related proteins are present and functionally active in human spermatozoa...
2016: Scientific Reports
Kara R Vogel, Garrett R Ainslie, K Michael Gibson
Recent studies have identified a role for supraphysiological gamma-aminobutyric acid (GABA) in the regulation of mechanistic target of rapamycin (mTOR), a protein kinase with pleiotropic roles in cellular development and homeostasis, including integration of growth factors and nutrient sensing and synaptic input in neurons (Lakhani et al. 2014; Vogel et al. 2015). Aldehyde dehydrogenase 5a1-deficient (aldh5a1 (-/-) ) mice, the murine orthologue of human succinic semialdehyde dehydrogenase deficiency (SSADHD), manifest increased GABA that disrupts mitophagy and increases mitochondria number with enhanced oxidant stress...
November 2016: Journal of Inherited Metabolic Disease
Zaira Aversa, Fabrizio Pin, Simone Lucia, Fabio Penna, Roberto Verzaro, Maurizio Fazi, Giuseppina Colasante, Andrea Tirone, Filippo Rossi Fanelli, Cesarina Ramaccini, Paola Costelli, Maurizio Muscaritoli
Basal rates of autophagy can be markedly accelerated by environmental stresses. Recently, autophagy has been involved in cancer-induced muscle wasting. Aim of this study has been to evaluate if autophagy is induced in the skeletal muscle of cancer patients. The expression (mRNA and protein) of autophagic markers has been evaluated in intraoperative muscle biopsies. Beclin-1 protein levels were increased in cachectic cancer patients, suggesting autophagy induction. LC3B-I protein levels were not significantly modified...
2016: Scientific Reports
Guan Gui, Shan-shan Meng, Lu-juan Li, Bin Liu, Hong-xia Liang, Chao-shen Huangfu
Nitrites play multiple characteristic functions in invasion and metastasis of hepatic cancer cells, but the exact mechanism is not yet known. Cancer cells can maintain the malignant characteristics via clearance of excess mitochondria by mitophagy. The purpose of this article was to determine the roles of nitrite, reactive oxygen species (ROS) and hypoxia inducing factor 1 alpha (HIF-1 α) in mitophagy of hepatic cancer cells. After exposure of human hepatocellular carcinoma SMMC-7721 cells to a serial concentrations of sodium nitrite for 24 h under normal oxygen, the maximal cell vitality was increased by 16 mg x (-1) sodium nitrite...
January 2016: Yao Xue Xue Bao, Acta Pharmaceutica Sinica
Inês O Gonçalves, Emanuel Passos, Cátia V Diogo, Sílvia Rocha-Rodrigues, Estela Santos-Alves, Paulo J Oliveira, António Ascensão, José Magalhães
Mitochondrial quality control and apoptosis have been described as key components in the pathogenesis of nonalcoholic steatohepatitis (NASH); exercise is recognized as a nonpharmacological strategy to counteract NASH-associated consequences. We aimed to analyze the effect of voluntary physical activity (VPA) and endurance training (ET) against NASH-induced mitochondrial permeability transition pore (mPTP) opening and mitochondrial and cellular quality control deleterious alterations. Forty-eight male Sprague-Dawley rats were divided into standard-diet sedentary (SS, n = 16), standard-diet VPA (n = 8), high-fat diet sedentary (HS, n = 16), and high-fat diet VPA (n = 8)...
March 2016: Applied Physiology, Nutrition, and Metabolism, Physiologie Appliquée, Nutrition et Métabolisme
Chounghun Kang, Li Li Ji
Loss of mitochondrial structural and functional integrity plays a critical role in the pathogenesis of muscle disuse atrophy. Peroxisome proliferator-activated receptor γ coactivator 1-α (PGC-1α) has been suggested to modulate autophagy-lysosome pathway (mitophagy) during muscle atrophy, but clear evidence is still lacking. In the current study, we tested the hypothesis that overexpression of PGC-1α via in vivo transfection would ameliorate mitophagy in mouse tibialis anterior muscle subjected to two weeks of immobilization (IM), followed by remobilization (RM)...
April 2016: Free Radical Biology & Medicine
Bing Cheng, An Xu, Mengran Qiao, Qiao Wu, Wenyu Wang, Yide Mei, Mian Wu
Mitochondria selective autophagy, known as mitophagy, plays a pivotal role in several biological processes, such as elimination of the damaged mitochondria, removal of the mitochondria from immature red blood cells and sperm. The defects in mitophagy are associated with a wide spectrum of human diseases, including neurodegenerative disease, aging, cardiac disease and autoimmune disease. However, the mechanism underlying mitophagy remains largely unclear. Here, we report the characterization of a novel splice variant of BECN1/Beclin 1, BECN1s, which is produced by an alternative splicing mechanism...
November 2, 2015: Autophagy
F Radogna, C Cerella, A Gaigneaux, C Christov, M Dicato, M Diederich
A limiting factor in the therapeutic outcome of children with high-risk neuroblastoma is the intrinsic and acquired resistance to common chemotherapeutic treatments. Here we investigated the molecular mechanisms by which the hemisynthetic cardiac glycoside UNBS1450 overcomes this limitation and induces differential cell death modalities in both neuroblastic and stromal neuroblastoma through stimulation of a cell-type-specific autophagic response eventually leading to apoptosis or necroptosis. In neuroblastic SH-SY5Y cells, we observed a time-dependent production of reactive oxygen species that affects lysosomal integrity inducing lysosome-associated membrane protein 2 degradation and cathepsin B and L activation...
July 21, 2016: Oncogene
Thomas Neill, Liliana Schaefer, Renato V Iozzo
Decorin is a prototypical small leucine-rich proteoglycan that epitomizes the multifunctional nature of this critical gene family. Soluble decorin engages multiple receptor tyrosine kinases within the target-rich environment of the tumor stroma and tumor parenchyma. Upon receptor binding, decorin initiates signaling pathways within endothelial cells downstream of VEGFR2 that ultimately culminate in a Peg3/Beclin 1/LC3-dependent autophagic program. Concomitant with autophagic induction, decorin blunts capillary morphogenesis and endothelial cell migration, thereby significantly compromising tumor angiogenesis...
February 1, 2016: Advanced Drug Delivery Reviews
Yongke Lu, Arthur I Cederbaum
Autophagy is an intracellular pathway by which lysosomes degrade and recycle long-lived proteins and cellular organelles. The effects of ethanol on autophagy are complex but recent studies have shown that autophagy serves a protective function against ethanol-induced liver injury. Autophagy was found to also be protective against CYP2E1-dependent toxicity in vitro in HepG2 cells which express CYP2E1 and in vivo in an acute alcohol/CYPE1-dependent liver injury model. The goal of the current report was to extend the previous in vitro and acute in vivo experiments to a chronic ethanol model to evaluate whether autophagy is also protective against CYP2E1-dependent liver injury in a chronic ethanol-fed mouse model...
2015: Biomolecules
Jian Lu, Yi Shen, Li-Jun Liu, Hui-Yin Qian, Chang-Lai Zhu
BACKGROUND: Recent experimental and clinical studies have indicated that the β-adrenergic effect of epinephrine significantly increases the severity of postresuscitation myocardial dysfunction. The aim of this study was to investigate whether the short-acting β1-selective adrenergic blocking agent, esmolol, would impact postresuscitation autophagy and mitophagy in cardiomyocytes in a rat cardiac arrest (CA) model. METHODS: CA was induced in Sprague Dawley rats by epicardial ventricular fibrillation for 5 minutes...
November 2015: Journal of Cardiovascular Pharmacology
Guo-Dong Ma, Yan-Huan Liu, Qing-Lai Zhang, Bao-Guo Zhang, Ning Zhao, Qiu-Ling Wang, Xiao-di Wang
AIM: The aim of this study is to investigate the effect of pre-endurance training on the prevention of alcohol-induced acute hepatic injury and on hepatic mitophagy. METHODS: Forty-eight male Sprague-Dawley rats were randomly divided into four groups: (1) control group, (2) 12-week exercise training group, (3) 5-day alcohol intake group, and (4) 12-week exercise training plus 5-day alcohol intake group. The rats were examined to determine the following: BCL2/adenovirus E1B 19 kDa protein-interacting protein 3 (BNIP3), hypoxia-inducible factor-1α (HIF-1α), cytochrome P450 2E1 (CYP2E1), alcohol dehydrogenase (ADH), microtubule-associated protein 1 light chain 3 (LC3II), Beclin1 mRNA and protein expressions, mitochondrial reactive oxygen species (ROS) production, mitochondrial thiobarbituric acid-reactive substances (TBARS) level, aconitase and ATP synthase activities, mitochondrial inner membrane potential, NADH/NAD(+) ratio, triglyceride (TG), the number of mtDNA and mitochondrial respiration functions in liver tissue, and serum ALT and AST...
July 2014: Hepatology International
R M Gorojod, A Alaimo, S Porte Alcon, C Pomilio, F Saravia, M L Kotler
Manganese (Mn) overexposure is frequently associated with the development of a neurodegenerative disorder known as Manganism. The Mn-mediated generation of reactive oxygen species (ROS) promotes cellular damage, finally leading to apoptotic cell death in rat astrocytoma C6 cells. In this scenario, the autophagic pathway could play an important role in preventing cytotoxicity. In the present study, we found that Mn induced an increase in the amount and total volume of acidic vesicular organelles (AVOs), a process usually related to the activation of the autophagic pathway...
October 2015: Free Radical Biology & Medicine
Jing Zou, Wenjiao Li, Anisha Misra, Fei Yue, Kun Song, Qi Chen, Guanghua Guo, Jinglin Yi, Jason T Kimata, Leyuan Liu
Tetherin has been characterized as a key factor that restricts viral particles such as HIV and hepatitis C virus on plasma membranes, acts as a ligand of the immunoglobulin-like transcript 7 (ILT7) receptor in tumor cells, and suppresses antiviral innate immune responses mediated by human plasmacytoid dendritic cells. However, the normal cellular function of Tetherin without viral infection is unknown. Here we show that Tetherin not only serves as a substrate of autophagy but itself regulates the initiation of autophagy...
March 13, 2015: Journal of Biological Chemistry
Anne-Emilie Declèves, Kumar Sharma, Joseph Satriano
Background: Kidney ischemia-reperfusion is a form of acute kidney injury resulting in a cascade of cellular events prompting rapid cellular damage and suppression of kidney function. A cellular response to ischemic stress is the activation of AMP-activated protein kinase (AMPK), where AMPK induces a number of homeostatic and renoprotective mechanisms, including autophagy. However, whether autophagy is beneficial or detrimental in ischemia-reperfusion remains controversial. We investigated the effects of agonist induction of AMPK activity on autophagy and cell stress proteins in the model of kidney ischemia-reperfusion...
December 6, 2014: Nephron. Experimental Nephrology
Alan L Chang, Allison Ulrich, Hagir B Suliman, Claude A Piantadosi
Oxidative mitochondrial damage is closely linked to inflammation and cell death, but low levels of reactive oxygen and nitrogen species serve as signals that involve mitochondrial repair and resolution of inflammation. More specifically, cytoprotection relies on the elimination of damaged mitochondria by selective autophagy (mitophagy) during mitochondrial quality control. This aim of this study was to identify and localize mitophagy in the mouse lung as a potentially upregulatable redox response to Staphylococcus aureus sepsis...
January 2015: Free Radical Biology & Medicine
Shaohua Chang, Gongyi Ren, Robert D Steiner, Louise Merkens, Jean-Baptiste Roullet, Zeljka Korade, Paul J DiMuzio, Thomas N Tulenko
Smith-Lemli-Opitz syndrome (SLOS) is a congenital, autosomal recessive metabolic and developmental disorder caused by mutations in the enzyme which catalyzes the reduction of 7-dehydrocholesterol (7DHC) to cholesterol. Herein we show that dermal fibroblasts obtained from SLOS children display increased basal levels of LC3B-II, the hallmark protein signifying increased autophagy. The elevated LC3B-II is accompanied by increased beclin-1 and cellular autophagosome content. We also show that the LC3B-II concentration in SLOS cells is directly proportional to the cellular concentration of 7DHC, suggesting that the increased autophagy is caused by 7DHC accumulation secondary to defective DHCR7...
2014: Molecular Genetics and Metabolism Reports
Agnieszka K Biala, Lorrie A Kirshenbaum
To date, one of the most intriguing and compelling concepts to impact contemporary cell biology is the notion that cell fate is "programmed" or genetically controlled. Indeed, the regulation of cell fate is crucial for embryonic development, and tissue homeostasis. Given the importance of removing damaged or irreversibly injured cells from the body, it is not surprising that defects in the regulatory mechanisms that govern cell death and/or survival more generally have been implicated in a number of human pathologies including cancer, neurodegenerative diseases, and cardiac failure...
November 2014: Trends in Cardiovascular Medicine
Emilie Hollville, Richard G Carroll, Sean P Cullen, Seamus J Martin
Mitophagy facilitates the selective elimination of impaired or depolarized mitochondria through targeting the latter to autophagosomes. Parkin becomes localized to depolarized mitochondria in a PINK1-dependent manner and polyubiquitinates multiple mitochondrial outer membrane proteins. This permits ubiquitin-binding proteins (e.g., p62 and NBR1) to target impaired mitochondria to autophagosomes via Atg8/LC3II. Bcl-2 family proteins regulate mitochondrial outer membrane permeabilization during apoptosis and can also influence macroautophagy via interactions with Beclin-1...
August 7, 2014: Molecular Cell
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