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ATG5 mitophagy

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https://www.readbyqxmd.com/read/28577568/pirfenidone-inhibits-myofibroblast-differentiation-and-lung-fibrosis-development-during-insufficient-mitophagy
#1
Yusuke Kurita, Jun Araya, Shunsuke Minagawa, Hiromichi Hara, Akihiro Ichikawa, Nayuta Saito, Tsukasa Kadota, Kazuya Tsubouchi, Nahoko Sato, Masahiro Yoshida, Kenji Kobayashi, Saburo Ito, Yu Fujita, Hirofumi Utsumi, Haruhiko Yanagisawa, Mitsuo Hashimoto, Hiroshi Wakui, Yutaka Yoshii, Takeo Ishikawa, Takanori Numata, Yumi Kaneko, Hisatoshi Asano, Makoto Yamashita, Makoto Odaka, Toshiaki Morikawa, Katsutoshi Nakayama, Kazuyoshi Kuwano
BACKGROUND: Pirfenidone (PFD) is an anti-fibrotic agent used to treat idiopathic pulmonary fibrosis (IPF), but its precise mechanism of action remains elusive. Accumulation of profibrotic myofibroblasts is a crucial process for fibrotic remodeling in IPF. Recent findings show participation of autophagy/mitophagy, part of the lysosomal degradation machinery, in IPF pathogenesis. Mitophagy has been implicated in myofibroblast differentiation through regulating mitochondrial reactive oxygen species (ROS)-mediated platelet-derived growth factor receptor (PDGFR) activation...
June 2, 2017: Respiratory Research
https://www.readbyqxmd.com/read/28521613/how-autophagy-eats-large-mitochondria-autophagosome-formation-coupled-with-mitochondrial-fragmentation
#2
Shun-Ichi Yamashita, Tomotake Kanki
Mitochondrial autophagy (mitophagy) is thought to be a multi-step pathway wherein mitochondria are first divided into small fragments, which are subsequently recognized by the phagophore. DNM1L (dynamin 1 like) plays a pivotal role in mitochondrial division; however, its role in mitophagy remains controversial. In our recent study, we examined the contribution of DNM1L to mitophagy and showed that mitophagy and mitochondrial division occur even in DNM1L-defective cells. Furthermore, time-lapse imaging of mitophagy showed that DNM1L-independent mitochondrial division occurs concomitantly with autophagosome formation...
May 4, 2017: Autophagy
https://www.readbyqxmd.com/read/28500249/maternal-high-fat-diet-induces-metabolic-stress-response-disorders-in-offspring-hypothalamus
#3
Long The Nguyen, Sonia Saad, Yi Tan, Carol Pollock, Hui Chen
Maternal obesity has been shown to increase the risk of obesity and related disorders in the offspring, which has been partially attributed to changes of appetite regulators in the offspring hypothalamus. On the other hand, endoplasmic reticulum (ER) stress and autophagy have been implicated in hypothalamic neuropeptide dysregulation, thus may also play important roles in such transgenerational effect.  In this study, we show that offspring born to HFD-fed dams showed significantly increased body weight and glucose intolerance, adiposity and plasma triglyceride level at weaning...
May 12, 2017: Journal of Molecular Endocrinology
https://www.readbyqxmd.com/read/28456949/monitoring-of-atg5-independent-mitophagy
#4
Satoko Arakawa, Shinya Honda, Satoru Torii, Masatsune Tsujioka, Shigeomi Shimizu
Mitophagy is a mitochondrial quality control mechanism where damaged and surplus mitochondria are removed by autophagy. There are at least two different mammalian autophagy pathways: the Atg5-dependent conventional pathway and an Atg5-independent alternative pathway; the latter is involved in the erythrocyte mitophagy. In this chapter we describe the various experimental approaches to assess Atg5-indepedndent mitophagy in mammalian cells.
April 30, 2017: Methods in Molecular Biology
https://www.readbyqxmd.com/read/28358377/mitochondrial-complex-i-inhibition-triggers-a-mitophagy-dependent-ros-increase-leading-to-necroptosis-and-ferroptosis-in-melanoma-cells
#5
Farhan Basit, Lisanne Mpe van Oppen, Laura Schöckel, Hasse M Bossenbroek, Sjenet E van Emst-de Vries, Johannes Cw Hermeling, Sander Grefte, Charlotte Kopitz, Melanie Heroult, Peter Hgm Willems, Werner Jh Koopman
Inhibition of complex I (CI) of the mitochondrial respiratory chain by BAY 87-2243 ('BAY') triggers death of BRAF(V600E) melanoma cell lines and inhibits in vivo tumor growth. Here we studied the mechanism by which this inhibition induces melanoma cell death. BAY treatment depolarized the mitochondrial membrane potential (Δψ), increased cellular ROS levels, stimulated lipid peroxidation and reduced glutathione levels. These effects were paralleled by increased opening of the mitochondrial permeability transition pore (mPTP) and stimulation of autophagosome formation and mitophagy...
March 30, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28292026/catalpol-protects-glucose-deprived-rat-embryonic-cardiac-cells-by-inducing-mitophagy-and-modulating-estrogen-receptor
#6
Chao Lin, Ying Lu, Xiaojing Yan, Xiang Wu, Meiyu Kuai, Xin Sun, Qi Chen, Xueyun Kong, Zhaoguo Liu, Yuping Tang, Yi Jing, Yu Li, Qichun Zhang, Huimin Bian
Catalpol, a bioactive component from Rehmannia glutinosa (Di Huang), has been widely used to protect cardiomyocytes against myocardial ischemia. The aim of the present study was to investigate the anti-apoptotic and anti-oxidative effects of Catalpol on glucose-starved H9c2 cells for cardio-protection and to elucidate the underlying mechanisms. Here, we showed that Catalpol protected the glucose-starved H9c2 cells through reducing apoptosis and attenuating oxidative damage. Moreover, the increases of autophagic lysosomes, LC3, autophagic flux and autophagic vacuole were observed in Catalpol-treated cells using flow cytometer and fluorescence microscope...
May 2017: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/27633131/autophagy-related-proteins-are-functionally-active-in-human-spermatozoa-and-may-be-involved-in-the-regulation-of-cell-survival-and-motility
#7
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...
September 16, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27413105/perfluorooctane-sulfonate-induces-autophagy-dependent-apoptosis-through-spinster-1-mediated-lysosomal-mitochondrial-axis-and-impaired-mitophagy
#8
Xiaofeng Yao, Shanshan Sha, Yuexia Wang, Xiance Sun, Jun Cao, Jian Kang, Liping Jiang, Min Chen, Yufang Ma
Lysosomal membrane permeabilization (LMP) and subsequently impaired autophagosome degradation was induced in HepG2 cells after treatment with perfluorooctane sulfonate (PFOS) for 24 h in our previous studies. We found that treatment of HepG2 cells with PFOS-induced autophagosome formation at earlier stage (6 h) of treatment in this study. The autophagosome formation inhibitor 3-methyladenine (3-MA) was able to relieve PFOS-induced LMP and release of cathepsin D in HepG2 cells. Knockdown of Spinster 1, a lysosomal membrane permease, attenuated PFOS-induced LMP in HepG2 cells...
September 2016: Toxicological Sciences: An Official Journal of the Society of Toxicology
https://www.readbyqxmd.com/read/27334109/the-pink1-synphilin-1-and-siah-1-complex-constitutes-a-novel-mitophagy-pathway
#9
Raymonde Szargel, Vered Shani, Fatimah Abd Elghani, Lucy N Mekies, Esti Liani, Ruth Rott, Simone Engelender
PTEN-induced putative kinase 1 (PINK1) and parkin are mutated in familial forms of Parkinson's disease and are important in promoting the mitophagy of damaged mitochondria. In this study, we showed that synphilin-1 interacted with PINK1 and was recruited to the mitochondria. Once in the mitochondria, it promoted PINK1-dependent mitophagy, as revealed by Atg5 knockdown experiments and the recruitment of LC3 and Lamp1 to the mitochondria. PINK1-synphilin-1 mitophagy did not depend on PINK1-mediated phosphorylation of synphilin-1 and occurred in the absence of parkin...
August 15, 2016: Human Molecular Genetics
https://www.readbyqxmd.com/read/27082295/prolyl-4-hydroxylases-inhibitor-stabilizes-hif-1%C3%AE-and-increases-mitophagy-to-reduce-cell-death-after-experimental-retinal-detachment
#10
Haiyang Liu, Hong Zhu, Tong Li, Pengfei Zhang, Ning Wang, Xiaodong Sun
PURPOSE: This study investigated the neuroprotective effect against photoreceptor cell death using prolyl-4-hydroxylases inhibitor (PHI), an HIF-1α stabilizer, in experimental retinal detachment (RD). METHODS: RD was created in Brown Norway rats by subretinal injection of 1% sodium hyaluronate. FG-4592 (a PHI, 25 mg/kg) or a vehicle was administered every 2 days with retro-orbital injection. Photoreceptor death was evaluated by TdT-dUTP terminal nick-end labeling (TUNEL) assay 3 days after RD and by the thickness of the outer nuclear layer 7 days after RD...
April 2016: Investigative Ophthalmology & Visual Science
https://www.readbyqxmd.com/read/26859293/galectin-1-induced-autophagy-facilitates-cisplatin-resistance-of-hepatocellular-carcinoma
#11
Yu-Chi Su, Goutham Venkata Naga Davuluri, Cheng-Hao Chen, Dong-Che Shiau, Chien-Chin Chen, Chia-Ling Chen, Yee-Shin Lin, Chih-Peng Chang
Hepatocellular carcinoma (HCC) is one of the most common cancers in Taiwan. Although chemotherapy is the primary treatment for HCC patients, drug resistance often leads to clinical failure. Galectin-1 is a beta-galactoside binding lectin which is up-regulated in HCC patients and promotes tumor growth by mediating cancer cell adhesion, migration and proliferation, but its role in chemoresistance of HCC is poorly understood. In this study we found that galectin-1 is able to lead to chemoresistance against cisplatin treatment, and subsequent inhibition has reversed the effect of cell death in HCC cells...
2016: PloS One
https://www.readbyqxmd.com/read/26773440/hemin-induces-mitophagy-in-a-leukemic-erythroblast-cell-line
#12
Claudio Marcelo Fader, Betiana Nebaí Salassa, Rubén Adrián Grosso, Agustín Nicolás Vergara, María Isabel Colombo
BACKGROUND INFORMATION: In eukaryotic cells, autophagy is considered a lysosomal catabolic process which participates in the degradation of intracellular components in a vacuolar structure termed autolysosome. This pathway plays a significant role in the erythropoiesis process, contributing to the clearance of some organelles (such as mitochondria) that are not necessary in the mature red blood cells. Nevertheless, the role of autophagy in erythrocyte maturation has not been fully established...
April 2016: Biology of the Cell
https://www.readbyqxmd.com/read/26640148/cell-type-dependent-ros-and-mitophagy-response-leads-to-apoptosis-or-necroptosis-in-neuroblastoma
#13
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
https://www.readbyqxmd.com/read/26549682/measuring-in-vivo-mitophagy
#14
Nuo Sun, Jeanho Yun, Jie Liu, Daniela Malide, Chengyu Liu, Ilsa I Rovira, Kira M Holmström, Maria M Fergusson, Young Hyun Yoo, Christian A Combs, Toren Finkel
Alterations in mitophagy have been increasingly linked to aging and age-related diseases. There are, however, no convenient methods to analyze mitophagy in vivo. Here, we describe a transgenic mouse model in which we expressed a mitochondrial-targeted form of the fluorescent reporter Keima (mt-Keima). Keima is a coral-derived protein that exhibits both pH-dependent excitation and resistance to lysosomal proteases. Comparison of a wide range of primary cells and tissues generated from the mt-Keima mouse revealed significant variations in basal mitophagy...
November 19, 2015: Molecular Cell
https://www.readbyqxmd.com/read/26292183/autophagy-supports-color-vision
#15
Zhenqing Zhou, Frans Vinberg, Frank Schottler, Teresa A Doggett, Vladimir J Kefalov, Thomas A Ferguson
Cones comprise only a small portion of the photoreceptors in mammalian retinas. However, cones are vital for color vision and visual perception, and their loss severely diminishes the quality of life for patients with retinal degenerative diseases. Cones function in bright light and have higher demand for energy than rods; yet, the mechanisms that support the energy requirements of cones are poorly understood. One such pathway that potentially could sustain cones under basal and stress conditions is macroautophagy...
2015: Autophagy
https://www.readbyqxmd.com/read/26272043/myristoylation-confers-noncanonical-ampk-functions-in-autophagy-selectivity-and-mitochondrial-surveillance
#16
Jiyong Liang, Zhi-Xiang Xu, Zhiyong Ding, Yiling Lu, Qinghua Yu, Kaitlin D Werle, Ge Zhou, Yun-Yong Park, Guang Peng, Michael J Gambello, Gordon B Mills
AMP-activated protein kinase (AMPK) plays a central role in cellular energy sensing and bioenergetics. However, the role of AMPK in surveillance of mitochondrial damage and induction of mitophagy remains unclear. We demonstrate herein that AMPK is required for efficient mitophagy. Mitochondrial damage induces a physical association of AMPK with ATG16-ATG5-12 and an AMPK-dependent recruitment of the VPS34 and ATG16 complexes with the mitochondria. Targeting AMPK to the mitochondria is both sufficient to induce mitophagy and to promote cell survival...
August 14, 2015: Nature Communications
https://www.readbyqxmd.com/read/26240184/mit-tfe-transcription-factors-are-activated-during-mitophagy-downstream-of-parkin-and-atg5
#17
Catherine L Nezich, Chunxin Wang, Adam I Fogel, Richard J Youle
The kinase PINK1 and ubiquitin ligase Parkin can regulate the selective elimination of damaged mitochondria through autophagy (mitophagy). Because of the demand on lysosomal function by mitophagy, we investigated a role for the transcription factor EB (TFEB), a master regulator of lysosomal biogenesis, in this process. We show that during mitophagy TFEB translocates to the nucleus and displays transcriptional activity in a PINK1- and Parkin-dependent manner. MITF and TFE3, homologues of TFEB belonging to the same microphthalmia/transcription factor E (MiT/TFE) family, are similarly regulated during mitophagy...
August 3, 2015: Journal of Cell Biology
https://www.readbyqxmd.com/read/26071643/ischemia-induced-autophagy-contributes-to-neurodegeneration-in-cerebellar-purkinje-cells-in-the-developing-rat-brain-and-in-primary-cortical-neurons-in-vitro
#18
Alicia K Au, Yaming Chen, Lina Du, Craig M Smith, Mioara D Manole, Sirine A Baltagi, Charleen T Chu, Rajesh K Aneja, Hülya Bayır, Patrick M Kochanek, Robert S B Clark
Increased autophagy/mitophagy is thought to contribute to cerebellar dysfunction in Purkinje cell degeneration mice. Intriguingly, cerebellar Purkinje cells are highly vulnerable to hypoxia-ischemia (HI), related at least in part to their high metabolic activity. Whether or not excessive or supraphysiologic autophagy plays a role in Purkinje cell susceptibility to HI is unknown. Accordingly, we evaluated the role of autophagy in the cerebellum after global ischemia produced by asphyxial cardiac arrest in postnatal day (PND) 16-18 rats, using siRNA-targeted inhibition of Atg7, necessary for microtubule-associated protein light chain 3-II (LC3-II) and Atg12-Atg5 complex formation...
September 2015: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/26048236/markers-of-autophagy-are-adapted-to-hyperglycaemia-in-skeletal-muscle-in-type-2-diabetes
#19
Rikke Kruse, Birgitte F Vind, Stine J Petersson, Jonas M Kristensen, Kurt Højlund
AIMS/HYPOTHESIS: Autophagy is a catabolic process that maintains cellular homeostasis by degradation of protein aggregates and selective removal of damaged organelles, e.g. mitochondria (mitophagy). Insulin resistance in skeletal muscle has been linked to mitochondrial dysfunction and altered protein metabolism. Here, we investigated whether abnormalities in autophagy are present in human muscle in obesity and type 2 diabetes. METHODS: Using a case-control design, skeletal muscle biopsies obtained in the basal and insulin-stimulated states from patients with type 2 diabetes during both euglycaemia and hyperglycaemia, and from glucose-tolerant lean and obese individuals during euglycaemia, were used for analysis of mRNA levels, protein abundance and phosphorylation of autophagy-related proteins...
September 2015: Diabetologia
https://www.readbyqxmd.com/read/26018823/mitochondrial-outer-membrane-e3-ligase-mul1-ubiquitinates-ulk1-and-regulates-selenite-induced-mitophagy
#20
Jie Li, Wei Qi, Guo Chen, Du Feng, Jinhua Liu, Biao Ma, Changqian Zhou, Chenglong Mu, Weilin Zhang, Quan Chen, Yushan Zhu
Mitochondria serve as membrane sources and signaling platforms for regulating autophagy. Accumulating evidence has also shown that damaged mitochondria are removed through both selective mitophagy and general autophagy in response to mitochondrial and oxidative stresses. Protein ubiquitination through mitochondrial E3 ligases plays an integrative role in mitochondrial outer membrane protein degradation, mitochondrial dynamics, and mitophagy. Here we showed that MUL1, a mitochondria-localized E3 ligase, regulates selenite-induced mitophagy in an ATG5 and ULK1-dependent manner...
2015: Autophagy
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