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Mitochondrial dysfunction

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https://www.readbyqxmd.com/read/28346709/synthetic-%C3%AE-nitrostyrene-derivative-cyt-rx20-as-inhibitor-of-oral-cancer-cell-proliferation-and-tumor-growth-through-glutathione-suppression-and-reactive-oxygen-species-induction
#1
Yen-Yun Wang, Yuk-Kwan Chen, Ya-Ling Hsu, Wen-Chin Chiu, Chun-Hao Tsai, Stephen Chu-Sung Hu, Pei-Wen Hsieh, Shyng-Shiou F Yuan
BACKGROUND: The β-nitrostyrene family possesses anticancer properties. In this study, β-nitrostyrene derivative CYT-Rx20 (3'-hydroxy-4'-methoxy-β-methyl-β-nitrostyrene) was synthesized and investigated its anticancer activity in oral cancer. METHODS: Anticancer activity of CYT-Rx20 and the underlying mechanisms were analyzed using cell viability assay, reactive oxygen species (ROS) generation assay, fluorescence-activated cell sorter analysis, annexin V staining, comet assay, glutathione (GSH)/glutathione disulfide (GSSG) ratio, immunoblotting, soft agar assay, nude mice xenograft study, and immunohistochemistry...
March 27, 2017: Head & Neck
https://www.readbyqxmd.com/read/28346483/effect-of-mir-146-targeted-hdmcp-up-regulation-in-the-pathogenesis-of-nonalcoholic-steatohepatitis
#2
Xi Jin, Jiang Liu, Yi-Peng Chen, Zun Xiang, Jie-Xia Ding, You-Ming Li
BACKGROUNDS/AIMS: Mitochondrial dysfunction plays an important role inthe pathogenesis of nonalcoholic steatohepatitis (NASH), where uncoupling protein (UCP) is actively involved. We previously reported the uncoupling activity of HDMCP and its role in liver steatosis. We now aim to investigate the degree and therapeutic effect of HDMCP in NASH and the regulatory role of miR-146 on HDMCP. METHODS: NASH animal model was established by feeding BALB/c mice with MCD diet while L02 cell was cultured with high concentration of fatty acid (HFFA) for 72h to mimic the steatosis and inflammation of NASH in-vitro appearance...
2017: PloS One
https://www.readbyqxmd.com/read/28346481/edaravone-protects-against-hyperosmolarity-induced-oxidative-stress-and-apoptosis-in-primary-human-corneal-epithelial-cells
#3
Yanwei Li, Haifeng Liu, Wei Zeng, Jing Wei
An increase in the osmolarity of tears induced by excessive evaporation of the aqueous tear phase is a major pathological mechanism behind dry eye. Exposure of epithelial cells on the surface of the human eye to hyperosmolarity leads to oxidative stress, mitochondrial dysfunction, and apoptosis. Edaravone, a hydroxyl radical scavenging agent, is clinically used to reduce neuronal damage following ischemic stroke. In this study, we found that treatment with hyperosmotic media at 400 and 450 mOsM increased the levels of ROS and mitochondrial oxidative damage, which were ameliorated by edaravone treatment in a dose-dependent manner...
2017: PloS One
https://www.readbyqxmd.com/read/28345781/apoptotic-pathways-of-macrophages-within-osteolytic-interface-membrane-in-periprosthestic-osteolysis-after-total-hip-replacement
#4
Guoyin Liu, Ting Guo, Yong Zhang, Naicheng Liu, Jiangning Chen, Jianmin Chen, Junfeng Zhang, Jianning Zhao
Macrophage apoptosis in interface membrane, which occurs through either death receptor, mitochondrion, or endoplasmic reticulum (ER) stress pathways, has been suggested to play an important role in promoting osteolysis. However, how and why macrophage apoptosis originates and the correlation among these apoptotic pathways is not yet clear. The objective of this study was to identify the apoptotic mechanism of macrophages, and to explore the relationship between the apoptotic pathways and progression of osteolysis...
March 27, 2017: APMIS: Acta Pathologica, Microbiologica, et Immunologica Scandinavica
https://www.readbyqxmd.com/read/28345767/nlrp3-inflammasome-its-regulation-and-involvement-in-atherosclerosis
#5
REVIEW
Zahra Hoseini, Fatemeh Sepahvand, Bahman Rashidi, Amirhossein Sahebkar, Aria Masoudifar, Hamed Mirzaei
Inflammasomes are intracellular complexes involved in the innate immunity that convert proIL-1β and proIL-18 to mature forms and initiate pyroptosis via cleaving procaspase-1. The most well-known inflammasome is NLRP3. Several studies have indicated a decisive and important role of NLRP3 inflammasome, IL-1β, IL-18, and pyroptosis in atherosclerosis. Modern hypotheses introduce atherosclerosis as an inflammatory/lipid-based disease and NLRP3 inflammasome has been considered as a link between lipid metabolism and inflammation because crystalline cholesterol and oxidized low-density lipoprotein (oxLDL) (two abundant components in atherosclerotic plaques) activate NLRP3 inflammasome...
March 27, 2017: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/28345618/ptpip51-regulates-mouse-cardiac-ischemia-reperfusion-through-mediating-the-mitochondria-sr-junction
#6
Xue Qiao, Shi Jia, Jingjing Ye, Xuan Fang, Chenglin Zhang, Yangpo Cao, Chunling Xu, Lifang Zhao, Yi Zhu, Lu Wang, Ming Zheng
Protein tyrosine phosphatase interacting protein 51 (PTPIP51) participates in multiple cellular processes, and dysfunction of PTPIP51 is implicated in diseases such as cancer and neurodegenerative disorders. However, there is no functional evidence showing the physiological or pathological roles of PTPIP51 in the heart. We have therefore investigated the role and mechanisms of PTPIP51 in regulating cardiac function. We found that PTPIP51 was markedly upregulated in ischemia/reperfusion heart. Upregulation of PTPIP51 by adenovirus-mediated overexpression markedly increased the contact of mitochondria-sarcoplasmic reticulum (SR), elevated mitochondrial Ca(2+) uptake from SR release through mitochondrial Ca(2+)uniporter...
March 27, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28345337/light-up-mitophagy-in-live-cells-with-dual-functional-theranostic-phosphorescent-iridium-iii-complexes
#7
Mu-He Chen, Fang-Xin Wang, Jian-Jun Cao, Cai-Ping Tan, Liang-Nian Ji, Zong-Wan Mao
Phosphorescent Ir(III) complexes are ideal candidates to construct novel multifunctional theranostic platforms that enable the integration of imaging capabilities and anticancer properties. Selective autophagy of mitochondria, termed mitophagy, is an important cellular process that selectively degrades dysfunctional mitochondria. Until now, the regulation of mitophagy is still poorly understood. Herein, we present two phosphorescent cyclometalated iridium(III) complexes (Ir1 and Ir2) that can accumulate in mitochondria and induce mitophagy...
March 27, 2017: ACS Applied Materials & Interfaces
https://www.readbyqxmd.com/read/28344128/high-sucrose-induced-maternal-obesity-disrupts-ovarian-function-and-decreases-fertility-in-drosophila-melanogaster
#8
Rita T Brookheart, Alison R Swearingen, Christina A Collins, Laura M Cline, Jennifer G Duncan
As the obesity epidemic worsens, the prevalence of maternal obesity is expected to rise. Both high-fat and high-sucrose diets are known to promote maternal obesity and several studies have elucidated the molecular influence of high-fat feeding on female reproduction. However, to date, the molecular impact of a high-sucrose diet on maternal obesity remains to be investigated. Using our previously reported Drosophila high-sucrose maternal obesity model, we sought to determine how excess dietary sucrose impacted the ovary...
March 24, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28343296/ibuprofen-protects-from-cypermethrin-induced-changes-in-the-striatal-dendritic-length-and-spine-density
#9
Pratibha Tripathi, Ashish Singh, Lakshmi Bala, Devendra Kumar Patel, Mahendra Pratap Singh
Microgliosis and inflammation are major wrongdoers in cypermethrin-induced Parkinsonism along with oxidative stress, mitochondrial dysfunction and α-synuclein aggregation. Dopamine depletion could alter dendritic morphology, length and spine number in the striatum. Present study investigated the effect of ibuprofen on the dendritic morphology, length and spine density in cypermethrin PD model. Male pups were treated intraperitoneally with cypermethrin during postnatal days followed by adulthood to induce Parkinsonism using standard procedure along with controls...
March 25, 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/28342966/time-courses-of-post-injury-mitochondrial-oxidative-damage-and-respiratory-dysfunction-and-neuronal-cytoskeletal-degradation-in-a-rat-model-of-focal-traumatic-brain-injury
#10
Rachel L Hill, Indrapal N Singh, Juan A Wang, Edward D Hall
Traumatic brain injury (TBI) results in rapid reactive oxygen species (ROS) production and oxidative damage to essential brain cellular components leading to neuronal dysfunction and cell death. It is increasingly appreciated that a major player in TBI-induced oxidative damage is the reactive nitrogen species (RNS) peroxynitrite (PN) which is produced in large part in injured brain mitochondria. Once formed, PN decomposes into highly reactive free radicals that trigger membrane lipid peroxidation (LP) of polyunsaturated fatty acids (e...
March 23, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28341344/propofol-affinity-to-mitochondrial-membranes-does-not-alter-mitochondrial-function
#11
Luís M Félix, Fernando Correia, Pedro A Pinto, Sónia P Campos, Telma Fernandes, Romeu Videira, M M Oliveira, Francisco P Peixoto, Luís M Antunes
The molecular mechanisms of hepatotoxicity after propofol anaesthesia have not been fully elucidated, although there is a relation with mitochondrial dysfunction. The action of propofol on mitochondrial hepatic functions in a rat model was evaluated by infusion for 4h with 25 and 62.5mg/kg/h propofol or 3.125ml/kg/h (vehicle). Liver mitochondrial respiratory rates were evaluated as well as mitochondrial transmembrane potential (ΔΨ), calcium fluxes, mitochondrial enzymatic activities (Complex I-V) and oxidative stress biomarkers (superoxide dismutase, catalase, glutathione reductase, glutathione S-transferase, lipid peroxidation and the oxidised/reduced glutathione ratio)...
March 22, 2017: European Journal of Pharmacology
https://www.readbyqxmd.com/read/28341289/long-term-culture-with-lipopolysaccharide-induces-dose-dependent-cytostatic-and-cytotoxic-effects-in-thp-1-monocytes
#12
Jennifer Mytych, Maria Romerowicz-Misielak, Marek Koziorowski
Monocytes act as a first line of defence against invading pathogens and their dysfunctions seem to be a key factor in many immune disorders. However, the data on mechanisms underlying these dysfunctions remain elusive. In this study, we evaluated the effects of long-term (168h) lipopolysaccharide exposure on monocytes at low density cultures (1×10(5)cells/ml). Treatment with low dose LPS (≤5μg/ml) resulted in oxidative stress induction followed by p21 pathway activation, permanent cell cycle arrest and SASP development...
March 21, 2017: Toxicology in Vitro: An International Journal Published in Association with BIBRA
https://www.readbyqxmd.com/read/28339814/modulating-oxidative-stress-relieves-stress-induced-behavioral-and-cognitive-impairments-in-rats
#13
Naimesh Solanki, Ankita Salvi, Gaurav Patki, Samina Salim
Background: Persistent psychological stress often leads to anxiety disorders and depression. Benzodiazepines and selective serotonin reuptake inhibitors are popular treatment options but have limited efficacy, supporting the need for alternative treatment. Based on our recent preclinical work suggesting a causal link between neurobehavioral deficits and elevated oxidative stress, we hypothesized that interventions that mitigate oxidative stress can attenuate/overcome neurobehavioral deficits...
February 24, 2017: International Journal of Neuropsychopharmacology
https://www.readbyqxmd.com/read/28338610/fructose-rich-diet-affects-mitochondrial-dna-damage-and-repair-in-rats
#14
Federica Cioffi, Rosalba Senese, Pasquale Lasala, Angela Ziello, Arianna Mazzoli, Raffaella Crescenzo, Giovanna Liverini, Antonia Lanni, Fernando Goglia, Susanna Iossa
Evidence indicates that many forms of fructose-induced metabolic disturbance are associated with oxidative stress and mitochondrial dysfunction. Mitochondria are prominent targets of oxidative damage; however, it is not clear whether mitochondrial DNA (mtDNA) damage and/or its lack of repair are events involved in metabolic disease resulting from a fructose-rich diet. In the present study, we evaluated the degree of oxidative damage to liver mtDNA and its repair, in addition to the state of oxidative stress and antioxidant defense in the liver of rats fed a high-fructose diet...
March 24, 2017: Nutrients
https://www.readbyqxmd.com/read/28338606/dystrophic-cardiomyopathy-potential-role-of-calcium-in-pathogenesis-treatment-and-novel-therapies
#15
REVIEW
Victoria P A Johnstone, Helena M Viola, Livia C Hool
Duchenne muscular dystrophy (DMD) is caused by defects in the DMD gene and results in progressive wasting of skeletal and cardiac muscle due to an absence of functional dystrophin. Cardiomyopathy is prominent in DMD patients, and contributes significantly to mortality. This is particularly true following respiratory interventions that reduce death rate and increase ambulation and consequently cardiac load. Cardiomyopathy shows an increasing prevalence with age and disease progression, and over 95% of patients exhibit dilated cardiomyopathy by the time they reach adulthood...
March 24, 2017: Genes
https://www.readbyqxmd.com/read/28338413/human-tissue-engineered-skeletal-muscle-myobundles-to-measure-oxygen-uptake-and-assess-mitochondrial-toxicity
#16
Brittany N J Davis, Jeffrey W Santoso, Michaela J Walker, Cindy S Cheng, Timothy R Koves, William E Kraus, George A Truskey
Mitochondrial dysfunction is responsible for the toxicity of a number of drugs. Current isolated mitochondria or cellular monoculture mitochondrial respiration measurement systems lack physiological relevance. Using a tissue engineering rather than cell- or mitochondria-based approach enables a more physiologically relevant detection of drug-induced mitochondrial impairment. To probe oxygen consumption and mitochondrial health, we assayed the bioenergetic profile of engineered three-dimensional human skeletal muscle myobundles derived from primary myoblasts...
March 24, 2017: Tissue Engineering. Part C, Methods
https://www.readbyqxmd.com/read/28337707/investigation-of-yeast-mitophagy-with-fluorescence-microscopy-and-western-blotting
#17
Sachiyo Nagumo, Koji Okamoto
Selective clearance of superfluous or dysfunctional mitochondria is a fundamental process that depends on the autophagic membrane trafficking pathways found in many cell types. This catabolic event, called mitophagy, is conserved from yeast to humans and serves to control mitochondrial quality and quantity. In budding yeast, degradation of mitochondria occurs under various physiological conditions, such as respiration at stationary phase, or starvation in a prolonged period. During these events, the transmembrane protein Atg32 localizes to the mitochondrial surface and plays a specific and essential role in yeast mitophagy...
March 24, 2017: Methods in Molecular Biology
https://www.readbyqxmd.com/read/28337258/neuroprotective-effect-of-win55-212-2-against-3-nitropropionic-acid-induced-toxicity-in-the-rat-brain-involvement-of-cb1-and-nmda-receptors
#18
Marisol Maya-López, Ana Laura Colín-González, Gabriela Aguilera, María Eduarda de Lima, Ana Colpo-Ceolin, Edgar Rangel-López, Juana Villeda-Hernández, Daniel Rembao-Bojórquez, Isaac Túnez, Armando Luna-López, Roberto Lazzarini-Lechuga, Viridiana Yazmín González-Puertos, Pedro Posadas-Rodríguez, Alejandro Silva-Palacios, Mina Königsberg, Abel Santamaría
The endocannabinoid system (ECS), and agonists acting on cannabinoid receptors (CBr), are known to regulate several physiological events in the brain, including modulatory actions on excitatory events probably through N-methyl-D-aspartate receptor (NMDAr) activity. Actually, CBr agonists can be neuroprotective. The synthetic CBr agonist WIN55,212-2 acts mainly on CB1 receptor. In turn, the mitochondrial toxin 3-nitropropionic acid (3-NP) produces striatal alterations in rats similar to those observed in the brain of Huntington's disease patients...
2017: American Journal of Translational Research
https://www.readbyqxmd.com/read/28337252/small-interfering-rna-targeting-mitochondrial-calcium-uniporter-improves-cardiomyocyte-cell-viability-in-hypoxia-reoxygenation-injury-by-reducing-calcium-overload
#19
Yuriana Oropeza-Almazán, Eduardo Vázquez-Garza, Héctor Chapoy-Villanueva, Guillermo Torre-Amione, Gerardo García-Rivas
Intracellular Ca(2+) mishandling is an underlying mechanism in hypoxia/reoxygenation (H/R) injury that results in mitochondrial dysfunction and cardiomyocytes death. These events are mediated by mitochondrial Ca(2+) (mCa(2+)) overload that is facilitated by the mitochondrial calcium uniporter (MCU) channel. Along this line, we evaluated the effect of siRNA-targeting MCU in cardiomyocytes subjected to H/R injury. First, cardiomyocytes treated with siRNA demonstrated a reduction of MCU expression by 67%, which resulted in significant decrease in mitochondrial Ca(2+) transport...
2017: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/28337125/neuronal-mitophagy-in-neurodegenerative-diseases
#20
REVIEW
Marta Martinez-Vicente
Neuronal homeostasis depends on the proper functioning of different quality control systems. All intracellular components are subjected to continuous turnover through the coordinated synthesis, degradation and recycling of their constituent elements. Autophagy is the catabolic mechanism by which intracellular cytosolic components, including proteins, organelles, aggregates and any other intracellular materials, are delivered to lysosomes for degradation. Among the different types of selective autophagy described to date, the process of mitophagy involves the selective autophagic degradation of mitochondria...
2017: Frontiers in Molecular Neuroscience
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