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https://www.readbyqxmd.com/read/28647372/delta-opioid-receptor-agonist-attenuates-lipopolysaccharide-induced-myocardial-injury-by-regulating-autophagy
#1
Pin Zhao, Jianke Kuai, Jinjian Gao, Li Sun, Yan Wang, Linong Yao
BACKGROUND: Previous studies have described the protective effects of DADLE on myocardial injury in sepsis. Recently, autophagy has been shown to be an innate defense mechanism in sepsis-related myocardial injury. However, whether DADLE has an pro-autophagic effect is yet to be elucidated. The present study aimed to investigate the effect of DADLE on the regulation of autophagy during sepsis. METHODS: Male mice were subjected to LPS or vehicle intraperitoneal injection...
June 21, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28647341/suppression-of-autophagic-flux-contributes-to-cardiomyocyte-death-by-activation-of-necroptotic-pathways
#2
Makoto Ogasawara, Toshiyuki Yano, Masaya Tanno, Koki Abe, Satoko Ishikawa, Takayuki Miki, Atsushi Kuno, Toshiyuki Tobisawa, Shingo Muratsubaki, Kouhei Ohno, Yuki Tatekoshi, Kei Nakata, Wataru Ohwada, Tetsuji Miura
BACKGROUND: The role of necroptosis in myocardial injury has not been fully characterized. Here we examined roles of mitochondrial permeability transition pore (mPTP) and autophagy in necroptosis of cardiomyocytes. METHODS AND RESULTS: In H9c2 cells, necroptosis was induced by treatment with TNF-α (TNF) and z-VAD-fmk (zVAD) for 24h, and necroptotic death was determined by LDH release (as % of total). TNF/zVAD increased LDH release from 16.6±4.3% to 60.6±2.7%, and the LDH release was suppressed by necrostatin-1 (29...
June 21, 2017: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/28646096/heat-stress-causes-dysfunctional-autophagy-in-oxidative-skeletal-muscle
#3
Alexandra J Brownstein, Shanthi Ganesan, Corey M Summers, Sarah Pearce, Benjamin J Hale, Jason W Ross, Nicholas Gabler, Jacob T Seibert, Robert P Rhoads, Lance H Baumgard, Joshua T Selsby
We have previously established that 24 h of environmental hyperthermia causes oxidative stress and have implicated mitochondria as likely contributors to this process. Given this, we hypothesized that heat stress would lead to increased autophagy/mitophagy and a reduction in mitochondrial content. To address this hypothesis pigs were housed in thermoneutral (TN; 20°C) or heat stress (35°C) conditions for 1- (HS1) or 3- (HS3) days and the red and white portions of the semitendinosus collected. We did not detect differences in glycolytic muscle...
June 2017: Physiological Reports
https://www.readbyqxmd.com/read/28641777/role-of-parl-pink1-parkin-pathway-in-adipocyte-differentiation
#4
Ming-Yuh Shiau, Pin-Shen Lee, Ying-Jyun Huang, Ching-Ping Yang, Chiao-Wan Hsiao, Kai-Yun Chang, Huan-Wen Chen, Yih-Hsin Chang
OBJECTIVE: Adipogenesis determines the number of adipocytes which is increased when individuals become obese. Mitochondria undergo remarkable morphological and functional changes during adipogenesis. PTEN-induced kinase 1 (PINK1) is pivotal to maintain mitochondrial homeostasis in neural cells. The present study aimed at investigating effects of PINK1 on adipogenesis and energy metabolism. METHODS: Expression of presenilin associated rhomboid-like protein (PARL), PINK1 and Parkin, as well as the interaction among these proteins was temporally examined during adipogenesis...
July 2017: Metabolism: Clinical and Experimental
https://www.readbyqxmd.com/read/28639297/autophagy-activation-not-pgc-1%C3%AE-may-mediate-exercise-induced-improvements-in-glucose-handling-during-diet-induced-obesity
#5
Megan E Rosa-Caldwell, Jacob L Brown, David E Lee, Thomas A Blackwell, Kyle W Turner, Lemuel A Brown, Richard A Perry, Wesley S Haynie, Tyrone A Washington, Nicholas P Greene
Prevalence of glucose intolerance is at alarming levels. Efforts to promote mitochondrial biogenesis through PGC-1α to mitigate glucose intolerance have been controversial. However, physical activity remains a primary means to alleviate the condition. PURPOSE: To determine combined effects of muscle-specific overexpression of PGC-1α and physical activity on glucose handling during diet-induced obesity. METHODS: Wild-type (WT, ∼20) and PGC-1α muscle transgenic (MCK-PGC-1α, ∼20) mice were given Western diet (WD) at 8 wks age and allowed to consume food ab libitum throughout the study...
June 21, 2017: Experimental Physiology
https://www.readbyqxmd.com/read/28634388/mito-xenophagic-killing-of-bacteria-is-coordinated-by-a-metabolic-switch-in-dendritic-cells
#6
Nadine Radomski, Danny Kägebein, Elisabeth Liebler-Tenorio, Axel Karger, Elke Rufer, Birke Andrea Tews, Stefanie Nagel, Rebekka Einenkel, Anne Müller, Annica Rebbig, Michael R Knittler
Chlamydiae are bacterial pathogens that grow in vacuolar inclusions. Dendritic cells (DCs) disintegrate these compartments, thereby eliminating the microbes, through auto/xenophagy, which also promotes chlamydial antigen presentation via MHC I. Here, we show that TNF-α controls this pathway by driving cytosolic phospholipase (cPLA)2-mediated arachidonic acid (AA) production. AA then impairs mitochondrial function, which disturbs the development and integrity of these energy-dependent parasitic inclusions, while a simultaneous metabolic switch towards aerobic glycolysis promotes DC survival...
June 20, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28634116/succinate-induced-neuronal-mitochondrial-fission-and-hexokinase-ii-malfunction-in-ischemic-stroke-therapeutical-effects-of-kaempferol
#7
Bin Wu, Hong Luo, Xu Zhou, Cai-Yi Cheng, Lin Lin, Bao-Lin Liu, Kang Liu, Ping Li, Hua Yang
Mitochondrial dysfunction is known as one of causative factors in ischemic stroke, leading to neuronal cell death. The present work was undertaken to investigate whether succinate induces neuron apoptosis by regulating mitochondrial morphology and function. In neurons, oxygen-glucose deprivation induced succinate accumulation due to the reversal of succinate dehydrogenase (SDH) activation, leading to mitochondrial fission. Kaempferol inhibited mitochondrial fission and maintained mitochondrial HK-II through activation of Akt, and thereby protected neurons from succinate-mediated ischemi injury...
June 17, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28630277/t-cell-intracellular-antigens-and-hu-antigen-r-antagonistically-modulate-mitochondrial-activity-and-dynamics-by-regulating-optic-atrophy-1-gene-expression
#8
Isabel Carrascoso, José Alcalde, Carmen Sánchez-Jiménez, Paloma González-Sánchez, José M Izquierdo
Mitochondria undergo frequent morphological changes to control their function. We show here that T-cell intracellular antigens (TIA1b/TIARb) and Hu antigen R (HuR) have antagonistic roles in mitochondrial function by modulating the expression of mitochondrial shaping proteins. Expression of TIA1b/TIARb alters the mitochondrial dynamic network by enhancing fission and clustering, which is accompanied by a decrease in respiration. By contrast, HuR expression promotes fusion and cristae remodeling and increases respiratory activity...
June 19, 2017: Molecular and Cellular Biology
https://www.readbyqxmd.com/read/28627624/pro-oxidant-activity-of-sulforaphane-and-cisplatin-potentiates-apoptosis-and-simultaneously-promotes-autophagy-in-malignant-mesothelioma-cells
#9
Yoon-Jin Lee, Sang-Han Lee
Sulforaphane (SFN) is an isothiocyanate compound derived from glucoraphanin, which is found in cruciferous vegetables, and has been heralded as a chemopreventive and/or chemotherapeutic agent. The present study investigated the effects of SFN on enhancing the anticancer role of cisplatin (cis-dichlorodiammineplatinum; CDDP) in H‑28 malignant mesothelioma cells. At concentrations demonstrating limited toxicity in MeT‑5A normal human mesothelial cells, combination treatment with the two compounds exhibited synergistic growth‑inhibiting and apoptosis‑promoting activities, as demonstrated by a series of proapoptotic events, including reactive oxygen species accumulation, loss of mitochondrial membrane potential, upregulation of p53 expression, increased B‑cell lymphoma 2 (Bcl‑2) associated X protein/Bcl‑2 ratio, activation of caspase‑3, the occurrence of a sub‑G0/G1 peak and an increase in cells with pyknotic and fragmented nuclei, Annexin V‑phycoerythrin‑positive staining and G2/M phase‑transition delay in the cell cycle...
June 15, 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/28626500/mitophagy-transcriptome-mechanistic-insights-into-polyphenol-mediated-mitophagy
#10
REVIEW
Sijie Tan, Esther Wong
Mitochondria are important bioenergetic and signalling hubs critical for myriad cellular functions and homeostasis. Dysfunction in mitochondria is a central theme in aging and diseases. Mitophagy, a process whereby damaged mitochondria are selectively removed by autophagy, plays a key homeostatic role in mitochondrial quality control. Upregulation of mitophagy has shown to mitigate superfluous mitochondrial accumulation and toxicity to safeguard mitochondrial fitness. Hence, mitophagy is a viable target to promote longevity and prevent age-related pathologies...
2017: Oxidative Medicine and Cellular Longevity
https://www.readbyqxmd.com/read/28626421/divergent-metabolic-regulation-of-autophagy-and-mtorc1-early-events-in-alzheimer-s-disease
#11
REVIEW
Mai A Shafei, Matthew Harris, Myra E Conway
Alzheimer's disease (AD) is a progressive disease associated with the production and deposition of amyloid β-peptide (Aβ) aggregates and neurofibrillary tangles, which lead to synaptic and neuronal damage. Reduced autophagic flux has been widely associated with the accumulation of autophagic vacuoles (AV), which has been proposed to contribute to aggregate build-up observed in AD. As such, targeting autophagy regulation has received wide review, where an understanding as to how this mechanism can be controlled will be important to neuronal health...
2017: Frontiers in Aging Neuroscience
https://www.readbyqxmd.com/read/28626114/thyroid-stimulating-hormone-stimulation-downregulates-autophagy-and-promotes-apoptosis-in-chondrocytes
#12
Wei Xin, Yue Yu, Yuan Ma, Yuan Gao, Ying Xu, Liyong Chen, Qiang Wan
Subclinical hypothyroidism (SCH) patients have normal thyroid hormone levels but increased thyroid stimulating hormone (TSH) level in serum. It has been reported that high TSH is related to abnormal skeletal development in mice with hypothyroidism. However, the cellular mechanism is not fully understood. In the present study, we aim to investigate the direct effects of TSH stimulation on chondrocytes, and the putative role of autophagy in this process. By using EdU incorporation assay and flow cytometry for mitochondrial membrane potential assay, we demonstrated deceased proliferation and promoted apoptosis in TSH stimulated primary mouse chondrocytes...
June 13, 2017: Endocrine Journal
https://www.readbyqxmd.com/read/28625916/er-stress-disturbs-sr-er-mitochondria-ca-2-transfer-implications-in-duchenne-muscular-dystrophy
#13
Marion Pauly, Claire Angebault-Prouteau, Haikel Dridi, Cécile Notarnicola, Valérie Scheuermann, Alain Lacampagne, Stefan Matecki, Jérémy Fauconnier
Besides its role in calcium (Ca(2+)) homeostasis, the sarco-endoplamic reticulum (SR/ER) controls protein folding and is tethered to mitochondria.Under pathophysiological conditions the unfolded protein response (UPR) is associated with disturbance in SR/ER-mitochondria crosstalk. Here, we investigated whether ER stress altered SR/ER-mitochondria links, Ca(2+) handling and muscle damage in WT (Wild Type) and mdx mice, the murine model of Duchenne Muscular Dystrophy (DMD). In WT mice, the SR/ER-mitochondria links were decreased in isolated FDB muscle fibers after injection of ER stress activator tunicamycin (TM)...
June 15, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28624623/mitochondrial-fission-forms-a-positive-feedback-loop-with-cytosolic-calcium-signaling-pathway-to-promote-autophagy-in-hepatocellular-carcinoma-cells
#14
Qichao Huang, Haiyan Cao, Lei Zhan, Xiacheng Sun, Gang Wang, Jibin Li, Xu Guo, Tingting Ren, Zhe Wang, Yinghua Lyu, Bingrong Liu, Jiaze An, Jinliang Xing
Both mitochondrial morphology and the level of cytosolic calcium [Ca(2+)]c are actively changed and play critical roles in a number of malignancies. However, whether communications existed between these two processes to ingeniously control the malignant phenotype are far from clear. We investigated the reciprocal regulation between mitochondrial fission and cytosolic calcium signaling in human hepatocellular carcinoma (HCC) cells. Furthermore, the underlying molecular mechanisms and the synergistic effect on autophagy were explored...
June 15, 2017: Cancer Letters
https://www.readbyqxmd.com/read/28624412/mild-hypothermia-protects-hippocampal-neurons-against-oxygen-glucose-deprivation-reperfusion-induced-injury-by-improving-lysosomal-function-and-autophagic-flux
#15
Tianen Zhou, Lian Liang, Yanran Liang, Tao Yu, Chaotao Zeng, Longyuan Jiang
Mild hypothermia has been proven to be useful to treat brain ischemia/reperfusion injury. However, the underlying mechanisms have not yet been fully elucidated. The present study was undertaken to determine whether mild hypothermia protects hippocampal neurons against oxygen-glucose deprivation/reperfusion(OGD/R)-induced injury via improving lysosomal function and autophagic flux. The results showed that OGD/R induced the occurrence of autophagy, while the acidic environment inside the lysosomes was altered...
June 15, 2017: Experimental Cell Research
https://www.readbyqxmd.com/read/28623712/deoxypodophyllotoxin-induces-cytoprotective-autophagy-against-apoptosis-via-inhibition-of-pi3k-akt-mtor-pathway-in-osteosarcoma-u2os-cells
#16
Sang-Hun Kim, Kyo-Min Son, Kwang-Youn Kim, Sun-Nyoung Yu, Sul-Gi Park, Young-Wook Kim, Hyo-Won Nam, Jeung-Tak Suh, Jae-Hoon Ji, Soon-Cheol Ahn
BACKGROUND: A natural compound deoxypodophyllotoxin (DPT) possesses potent anti-proliferative and anti-tumor properties on several cancer types. It triggers cell cycle arrest followed by apoptosis through various cellular processes. However, it is limited to the action mechanism of DPT-mediated cell death modes via apoptosis and autophagy. METHODS: Cell viability assay, morphological changes, annexin-V/propidium iodide (PI) assay, reactive oxygen species (ROS), acridine orange staining, and Western blot analyses were evaluated...
April 13, 2017: Pharmacological Reports: PR
https://www.readbyqxmd.com/read/28622296/bcl-2-family-integrating-stress-responses-at-the-er-to-control-cell-demise
#17
REVIEW
Philippe Pihán, Amado Carreras-Sureda, Claudio Hetz
In the last decade, the endoplasmic reticulum (ER) has emerged as a central organelle regulating the core mitochondrial apoptosis pathway. At the ER membrane, a variety of stress signals are integrated toward determining cell fate, involving a complex cross talk between key homeostatic pathways including the unfolded protein response, autophagy, calcium signaling and mitochondrial bioenergetics. In this context, key regulators of cell death of the BCL-2 and TMBIM/BI-1 family of proteins have relevant functions as stress rheostats mediated by the formation of distinct protein complexes that regulate the switch between adaptive and proapoptotic phases under stress...
June 16, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28622295/high-autophagic-flux-guards-esc-identity-through-coordinating-autophagy-machinery-gene-program-by-foxo1
#18
Pinglei Liu, Kun Liu, Haifeng Gu, Weixu Wang, Jiaqi Gong, Yingjie Zhu, Qian Zhao, Jiani Cao, Chunseng Han, Fei Gao, Quan Chen, Wei Li, Jianwei Jiao, Baoyang Hu, Qi Zhou, Tongbiao Zhao
Although much is known about transcriptional networks that control embryonic stem cell (ESC) self-renewal and differentiation, the metabolic regulation of ESC is less clear. Autophagy is a catabolic process that is activated under both stress and normal conditions to degrade damaged organelles and aggregated proteins, and thus plays pivotal roles in somatic and adult stem cell function. However, if and how ESCs harness autophagy to regulate stemness remains largely unknown. Recently, we have defined that autophagy is essential for mitochondrial homeostasis regulation in pluripotency acquirement and maintenance...
June 16, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28619984/mitochondrial-integrity-and-function-in-the-progression-of-early-pressure-overload-induced-left-ventricular-remodeling
#19
Antoine H Chaanine, K Sreekumaran Nair, Robert H Bergen, Katherine Klaus, Adam J Guenzel, Roger J Hajjar, Margaret M Redfield
BACKGROUND: Following pressure overload, compensatory concentric left ventricular remodeling (CR) variably transitions to eccentric remodeling (ER) and systolic dysfunction. Mechanisms responsible for this transition are incompletely understood. Here we leverage phenotypic variability in pressure overload-induced cardiac remodeling to test the hypothesis that altered mitochondrial homeostasis and calcium handling occur early in the transition from CR to ER, before overt systolic dysfunction...
June 15, 2017: Journal of the American Heart Association
https://www.readbyqxmd.com/read/28619032/the-role-of-intracellular-trafficking-of-cdse-zns-qds-on-their-consequent-toxicity-profile
#20
Bella B Manshian, Thomas F Martens, Karsten Kantner, Kevin Braeckmans, Stefaan C De Smedt, Jo Demeester, Gareth J S Jenkins, Wolfgang J Parak, Beatriz Pelaz, Shareen H Doak, Uwe Himmelreich, Stefaan J Soenen
BACKGROUND: Nanoparticle interactions with cellular membranes and the kinetics of their transport and localization are important determinants of their functionality and their biological consequences. Understanding these phenomena is fundamental for the translation of such NPs from in vitro to in vivo systems for bioimaging and medical applications. Two CdSe/ZnS quantum dots (QD) with differing surface functionality (NH2 or COOH moieties) were used here for investigating the intracellular uptake and transport kinetics of these QDs...
June 15, 2017: Journal of Nanobiotechnology
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