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L Hui, H Wu, T-W Wang, N Yang, X Guo, X-J Jang
PURPOSE: The purpose of our study was to investigate an underlying mechanism that hydrogen peroxide-induced mitophagy contributed to laryngeal cancer cells survivals under oxidative stress condition. METHODS: Tumor tissue and serum samples were collected from patients with laryngeal cancer. The Hep2 cell, a human laryngeal carcinoma cell, was used in in vitro experiments. The levels of lipid peroxidation were analyzed by ELISA. Knockdown of FUNDC1 was performed by RNAi...
October 3, 2018: Clinical & Translational Oncology
Alan Diot, Thomas Agnew, Jeremy Sanderson, Chunyan Liao, Janet Carver, Ricardo Pires das Neves, Rajeev Gupta, Yanping Guo, Caroline Waters, Sharon Seto, Matthew J Daniels, Eszter Dombi, Tiffany Lodge, Karl Morten, Suzannah A Williams, Tariq Enver, Francisco J Iborra, Marcela Votruba, Joanna Poulton
Background: Autosomal dominant optic atrophy (ADOA) is usually caused by mutations in the essential gene, OPA1. This encodes a ubiquitous protein involved in mitochondrial dynamics, hence tissue specificity is not understood. Dysregulated mitophagy (mitochondria recycling) is implicated in ADOA, being increased in OPA1 patient fibroblasts. Furthermore, autophagy may be increased in retinal ganglion cells (RGCs) of the OPA1Q285STOP mouse model. Aims: We developed a mouse model for studying mitochondrial dynamics in order to investigate mitophagy in ADOA...
2018: Frontiers in Cell and Developmental Biology
Jun Zhang, Bin Wang, Hong Wang, Hui He, Qiong Wu, Xia Qin, Xi Yang, Linmu Chen, Ge Xu, Zhiyi Yuan, Qiying Yi, Zhen Zou, Chao Yu
Copper oxide nanoparticles (CuONPs) have been widely used in the industrial and pharmaceutical fields; however, their toxicity profile is deeply concerning. Currently, nanomaterials-induced toxicity in the cardiovascular system is receiving increased attention. Our previous toxicological study found that lysosomal deposition of CuONPs triggered vascular endothelial cell death, indicating that the involvement of autophagic dysfunction was crucial for CuONPs-induced toxicity in human umbilical vein endothelial cells (HUVECs)...
September 21, 2018: Free Radical Biology & Medicine
Fabiana F Ferreira, Evelise M Nazari, Yara M R Müller
Methylmercury (MeHg) is a known neurodevelopmental toxicant, which causes changes in various structures of the central nervous system (CNS). However, ultrastructural studies of its effects on the developing CNS are still scarce. Here, we investigated the effect of MeHg on the ultrastructure of the cells in spinal cord layers. Chicken embryos at E3 were treated in ovo with 0.1 μ g MeHg/50 μ L saline solution and analyzed at E10. Then, we used transmission electron microscopy (TEM) to identify possible damage caused by MeHg to the structures and organelles of the spinal cord cells...
2018: Journal of Toxicology
Anthea Di Rita, Angelo Peschiaroli, Pasquale D Acunzo, Daniela Strobbe, Zehan Hu, Jens Gruber, Mads Nygaard, Matteo Lambrughi, Gerry Melino, Elena Papaleo, Jörn Dengjel, Said El Alaoui, Michelangelo Campanella, Volker Dötsch, Vladimir V Rogov, Flavie Strappazzon, Francesco Cecconi
The selective removal of undesired or damaged mitochondria by autophagy, known as mitophagy, is crucial for cellular homoeostasis, and prevents tumour diffusion, neurodegeneration and ageing. The pro-autophagic molecule AMBRA1 (autophagy/beclin-1 regulator-1) has been defined as a novel regulator of mitophagy in both PINK1/PARKIN-dependent and -independent systems. Here, we identified the E3 ubiquitin ligase HUWE1 as a key inducing factor in AMBRA1-mediated mitophagy, a process that takes place independently of the main mitophagy receptors...
September 14, 2018: Nature Communications
Carmen Teodorof-Diedrich, Stephen A Spector
HIV enters the central nervous system (CNS) during the early stages of infection and can cause neurological dysfunction including neurodegeneration and neurocognitive impairment. Specific autophagy responsible for removal of damaged mitochondria (mitophagy) and mitochondrial dynamics constitute neuronal mitochondrial quality control mechanisms, and are impaired in neurodegenerative disorders and numerous other diseases. Release of HIV proteins, gp120 and Tat, from infected cells is thought to play an important role in HIV-associated neurocognitive disorders (HAND), but the mechanism(s) leading to impairment are poorly understood...
August 29, 2018: Journal of Virology
Yang Yuan, Shan-Shan Pan, Dong-Feng Wan, Jiao Lu, Yue Huang
Previous studies have shown that early exercise preconditioning (EEP) imparts a protective effect on acute cardiovascular stress. However, how mitophagy participates in exercise preconditioning- (EP-) induced cardioprotection remains unclear. EEP may involve mitochondrial protection, which presumably crosstalks with predominant H2 O2 oxidative stress. Our EEP protocol involves four periods of 10 min running with 10 min recovery intervals. We added a period of exhaustive running and a pretreatment using phosphoinositide 3-kinase (PI3K)/autophagy inhibitor wortmannin to test this protective effect...
2018: Oxidative Medicine and Cellular Longevity
Zhanwei Zhang, Jianbai Yu
Mitochondrial dysfunction has been acknowledged as the key pathogenic mechanism in cerebral ischemia-reperfusion (IR) injury. Mitophagy is the protective system used to sustain mitochondrial homeostasis. However, the upstream regulator of mitophagy in response to brain IR injury is not completely understood. Nuclear receptor subfamily 4 group A member 1 (NR4A1) has been found to be associated with mitochondrial protection in a number of diseases. The aim of our study is to explore the functional role of NR4A1 in cerebral IR injury, with a particular focus on its influence on mitophagy...
October 2018: Neurochemical Research
Ana C Bento, Claudia C Bippes, Corina Kohler, Charles Hemion, Stephan Frank, Albert Neutzner
Clearance of damaged mitochondria through mitophagy is critical for maintaining mitochondrial fidelity and the prevention of neurodegeneration. Here, we report on the UBX domain-containing, p97/VCP cofactor UBXD1/UBXN6/UBXDC2 and its role in mitophagy. Recognizing depolarized mitochondria via its C-terminal UBX domain, UBXD1 translocates to mitochondria in a Parkin-dependent manner. During Parkin-independent mitophagy, UBXD1 shows no mitochondrial translocation. Once translocated, UBXD1 recruits p97 to mitochondria via a bipartite binding motif consisting of its N-terminal VIM and PUB domains...
August 17, 2018: Scientific Reports
Ching-Chi Chiu, Chin-Song Lu, Yi-Hsin Weng, Ying-Ling Chen, Ying-Zu Huang, Rou-Shayn Chen, Yi-Chuan Cheng, Yin-Cheng Huang, Yu-Chuan Liu, Szu-Chia Lai, Kun-Jun Lin, Yan-Wei Lin, Yu-Jie Chen, Chao-Lang Chen, Tu-Hsueh Yeh, Hung-Li Wang
PARK14 patients with homozygous (D331Y) PLA2G6 mutation display motor deficits of pure early-onset Parkinson's disease (PD). The aim of this study is to investigate the pathogenic mechanism of mutant (D331Y) PLA2G6-induced PD. We generated knockin (KI) mouse model of PARK14 harboring homozygous (D331Y) PLA2G6 mutation. Then, we investigated neuropathological and neurological phenotypes of PLA2G6D331Y/D331Y KI mice and molecular pathogenic mechanisms of (D331Y) PLA2G6-induced degeneration of substantia nigra (SN) dopaminergic neurons...
August 8, 2018: Molecular Neurobiology
Alex Von Schulze, Colin S McCoin, Chiemela Onyekere, Julie Allen, Paige Geiger, Gerald W Dorn, E Matthew Morris, John P Thyfault
KEY POINTS: Hepatic mitochondrial adaptations to physical activity may be regulated by mitochondrial biogenesis (PGC1α) and mitophagy (BNIP3). Additionally, these adaptations may be sex-dependent. Chronic increase in physical activity lowers basal mitochondrial respiratory capacity in mice. Female mice have higher hepatic electron transport system protein content, elevated respiratory capacity, lowered mitophagic flux, and emit less mitochondrial H2 O2 independent of physical activity...
July 31, 2018: Journal of Physiology
Wenhui Li, Yanjun Li, Sami Siraj, Haojie Jin, Yuyuan Fan, Xinrong Yang, Xiaowu Huang, Xiaohui Wang, Jun Wang, Lei Liu, Lei Du, Quan Chen
Mitochondria lie at the heart of innate immunity, and aberrant mitochondrial activity contributes to immune activation and chronic inflammatory diseases including liver cancers. Mitophagy is a selective process for removing dysfunctional mitochondria. The link between mitophagy and inflammation in tumorigenesis remains largely unexplored. We observed that FUNDC1, a previously characterized mitophagy receptor, accumulates in most human hepatocellular carcinomas (HCCs), and we thus explored the role of FUNDC1-mediated mitophagy in HCC initiation and progression in a mouse model in which HCC is induced by the chemical carcinogen diethylnitrosamine (DEN)...
July 27, 2018: Hepatology: Official Journal of the American Association for the Study of Liver Diseases
Zachary A Graham, Lauren Harlow, William A Bauman, Christopher P Cardozo
INTRODUCTION: Paralysis and unloading of skeletal muscle leads to a rapid loss in muscle size, function and oxidative capacity. The reduction in metabolic capability after disuse leads to dysregulation and increased breakdown of mitochondria by mitophagy. METHODS: Eight-week-old C57BL/6 male mice were given a sham surgery or sciatic nerve transection. Animals were euthanized at 7, 14, 21, or 35 days postsurgery. Whole gastrocnemius muscles were isolated from the animal, weighed and used for Western blotting...
October 2018: Muscle & Nerve
Nina Meyer, Svenja Zielke, Jonas B Michaelis, Benedikt Linder, Verena Warnsmann, Stefanie Rakel, Heinz D Osiewacz, Simone Fulda, Michel Mittelbronn, Christian Münch, Christian Behrends, Donat Kögel
In most cases, macroautophagy/autophagy serves to alleviate cellular stress and acts in a pro-survival manner. However, the effects of autophagy are highly contextual, and autophagic cell death (ACD) is emerging as an alternative paradigm of (stress- and drug-induced) cell demise. AT 101 ([-]-gossypol), a natural compound from cotton seeds, induces ACD in glioma cells as confirmed here by CRISPR/Cas9 knockout of ATG5 that partially, but significantly rescued cell survival following AT 101 treatment. Global proteomic analysis of AT 101-treated U87MG and U343 glioma cells revealed a robust decrease in mitochondrial protein clusters, whereas HMOX1 (heme oxygenase 1) was strongly upregulated...
2018: Autophagy
Britney N Lizama, Amy M Palubinsky, Vineeth A Raveendran, Annah M Moore, Joel D Federspiel, Simona G Codreanu, Daniel C Liebler, BethAnn McLaughlin
C-terminus of HSC70-interacting protein (CHIP, STUB1 ) is a ubiquitously expressed cytosolic E3-ubiquitin ligase. CHIP-deficient mice exhibit cardiovascular stress and motor dysfunction prior to premature death. This phenotype is more consistent with animal models in which master regulators of autophagy are affected rather than with the mild phenotype of classic E3-ubiquitin ligase mutants. The cellular and biochemical events that contribute to neurodegeneration and premature aging in CHIP KO models remain poorly understood...
June 22, 2018: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
Thomas Neill, Eva Andreuzzi, Zi-Xuan Wang, Stephen C Peiper, Maurizo Mongiat, Renato V Iozzo
Regulation of autophagy by proteolytically cleaved fragments of heparan sulfate proteoglycans is a novel and current research focus in tumor biology. Endorepellin is the C-terminal angiostatic fragment of the heparan sulfate proteoglycan perlecan and induces autophagy in endothelial cells. To further investigate this property, we used NanoString, a digital PCR platform for measuring pre-defined transcripts in biological samples to analyze a custom subset of 95 autophagy-related genes in human umbilical vein endothelial cells treated with ultrapure human recombinant endorepellin...
August 3, 2018: Journal of Biological Chemistry
Linliang Zhang, Yali Qin, Mingzhou Chen
Viral infection causes many physiological alterations in the host cell, and many of these alterations can affect the host mitochondrial network, including mitophagy induction. A substantial amount of literature has been generated that advances our understanding of the relationship between mitophagy and several viruses. Some viruses trigger mitophagy directly, and indirectly and control the mitophagic process via different strategies. This enables viruses to promote persistent infection and attenuate the innate immune responses...
2018: Autophagy
Huang Deyu, Cui Luqing, Liu Xianglian, Guo Pu, Lu Qirong, Wang Xu, Yuan Zonghui
T-2 toxin is the most toxic member of trichothecene mycotoxin. So far, the mechanism of mitochondrial toxicity and protective mechanism in mammalian cells against T-2 toxin are not fully understood. In this study, we aimed to investigate the cellular and mitochondrial toxicity of T-2 toxin, and the cellular protective mechanisms in rat pituitary GH3 cells. We showed that T-2 toxin significantly increased reactive oxygen species (ROS) and DNA damage and caused apoptosis in GH3 cells. T-2 toxin induced abnormal cell morphology, cytoplasm and nuclear shrinkage, nuclear fragmentation and formation of apoptotic bodies and autophagosomes...
October 1, 2018: Toxicology Letters
Chris Chin Wah Chen, Avigail T Erlich, Matthew J Crilly, David A Hood
The maintenance of muscle health with advancing age is dependent on mitochondrial homeostasis. While reductions in mitochondrial biogenesis have been observed with age, less is known regarding organelle degradation. Parkin is an E3 ubiquitin ligase implicated in mitophagy, but few studies have examined Parkin's contribution to mitochondrial turnover in muscle. Wild-type (WT) and Parkin knockout (KO) mice were used to delineate a role for Parkin-mediated mitochondrial degradation in aged muscle, in concurrence with exercise...
September 1, 2018: American Journal of Physiology. Endocrinology and Metabolism
Frédéric Checler, Thomas Goiran, Cristine Alves da Costa
The tumor suppressor TP53/p53 is a key protein in both neurodegenerative diseases and cancer. Thus, TP53-linked cell death appears exacerbated in several age-related neuropathologies, while TP53 mutation-associated phenotypes indicate a loss of function accounting for approximately half of cancers. Thus, TP53 plays a pivotal role in these phenotypically distinct pathologies, a hypothesis reinforced by recent epidemiological studies suggesting an opposite risk to develop one type of pathology relative to the other...
2018: Autophagy
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