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Mitophagy

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https://www.readbyqxmd.com/read/27913663/resistance-of-dynamin-related-protein-1-oligomers-to-disassembly-impairs-mitophagy-resulting-in-myocardial-inflammation-and-heart-failure
#1
Thomas J Cahill, Vincenzo Leo, Matthew Kelly, Alexander Stockenhuber, Nolan W Kennedy, Leyuan Bao, Grazia M Cereghetti, Andrew R Harper, Gabor Czibik, Chunyan Liao, Mohammed Bellahcene, Violetta Steeples, Sahar Ghaffari, Arash Yavari, Alice Mayer, Joanna Poulton, David J P Ferguson, Luca Scorrano, Nishani T Hettiarachchi, Chris Peers, John Boyle, R Blake Hill, Alison Simmons, Hugh Watkins, T Neil Dear, Houman Ashrafian
No abstract text is available yet for this article.
December 2, 2016: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/27913197/doxorubicin-induced-mitophagy-contributes-to-drug-resistance-in-cancer-stem-cells-from-hct8-human-colorectal-cancer-cells
#2
Chen Yan, Lan Luo, Chang-Ying Guo, Shinji Goto, Yoshishige Urata, Jiang-Hua Shao, Tao-Sheng Li
Cancer stem cells (CSCs) are known to be drug resistant. Mitophagy selectively degrades unnecessary or damaged mitochondria by autophagy during cellular stress. To investigate the potential role of mitophagy in drug resistance in CSCs, we purified CD133(+)/CD44(+) CSCs from HCT8 human colorectal cancer cells and then exposed to doxorubicin (DXR). Compared with parental cells, CSCs were more resistant to DXR treatment. Although DXR treatment enhanced autophagy levels in both cell types, the inhibition of autophagy by ATG7 silencing significantly increased the toxicity of DXR only in parental cells, not in CSCs...
November 30, 2016: Cancer Letters
https://www.readbyqxmd.com/read/27912065/phosphoribosylation-of-ubiquitin-promotes-serine-ubiquitination-and-impairs-conventional-ubiquitination
#3
Sagar Bhogaraju, Sissy Kalayil, Yaobin Liu, Florian Bonn, Thomas Colby, Ivan Matic, Ivan Dikic
Conventional ubiquitination involves the ATP-dependent formation of amide bonds between the ubiquitin C terminus and primary amines in substrate proteins. Recently, SdeA, an effector protein of pathogenic Legionella pneumophila, was shown to mediate NAD-dependent and ATP-independent ubiquitin transfer to host proteins. Here, we identify a phosphodiesterase domain in SdeA that efficiently catalyzes phosphoribosylation of ubiquitin on a specific arginine via an ADP-ribose-ubiquitin intermediate. SdeA also catalyzes a chemically and structurally distinct type of substrate ubiquitination by conjugating phosphoribosylated ubiquitin to serine residues of protein substrates via a phosphodiester bond...
December 1, 2016: Cell
https://www.readbyqxmd.com/read/27911343/pink1-parkin-and-mitochondrial-quality-control-what-can-we-learn-about-parkinson-s-disease-pathobiology
#4
Dominika Truban, Xu Hou, Thomas R Caulfield, Fabienne C Fiesel, Wolfdieter Springer
The first clinical description of Parkinson's disease (PD) will embrace its two century anniversary in 2017. For the past 30 years, mitochondrial dysfunction has been hypothesized to play a central role in the pathobiology of this devastating neurodegenerative disease. The identifications of mutations in genes encoding PINK1 (PTEN-induced kinase 1) and Parkin (E3 ubiquitin ligase) in familial PD and their functional association with mitochondrial quality control provided further support to this hypothesis. Recent research focused mainly on their key involvement in the clearance of damaged mitochondria, a process known as mitophagy...
November 30, 2016: Journal of Parkinson's Disease
https://www.readbyqxmd.com/read/27908782/adaptive-responses-of-neuronal-mitochondria-to-bioenergetic-challenges-roles-in-neuroplasticity-and-disease-resistance
#5
REVIEW
Sophia M Raefsky, Mark P Mattson
An important concept in neurobiology is "neurons that fire together, wire together" which means that the formation and maintenance of synapses is promoted by activation of those synapses. Very similar to the effects of the stress of exercise on muscle cells, emerging findings suggest that neurons respond to activity by activating signaling pathways (e.g., Ca(2+), CREB, PGC-1α, NF-κB) that stimulate mitochondrial biogenesis and cellular stress resistance. These pathways are also activated by aerobic exercise and food deprivation, two bioenergetic challenges of fundamental importance in the evolution of the brains of all mammals, including humans...
November 29, 2016: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/27907896/harnessing-human-adar2-for-rna-repair-recoding-a-pink1-mutation-rescues-mitophagy
#6
Jacqueline Wettengel, Philipp Reautschnig, Sven Geisler, Philipp J Kahle, Thorsten Stafforst
Site-directed A-to-I RNA editing is a technology for re-programming genetic information at the RNA-level. We describe here the first design of genetically encodable guideRNAs that enable the re-addressing of human ADAR2 toward specific sites in user-defined mRNA targets. Up to 65% editing yield has been achieved in cell culture for the recoding of a premature Stop codon (UAG) into tryptophan (UIG). In the targeted gene, editing was very specific. We applied the technology to recode a recessive loss-of-function mutation in PINK1 (W437X) in HeLa cells and showed functional rescue of PINK1/Parkin-mediated mitophagy, which is linked to the etiology of Parkinson's disease...
October 7, 2016: Nucleic Acids Research
https://www.readbyqxmd.com/read/27907115/brucella-melitensis-16m-regulates-the-effect-of-air-domain-on-inflammatory-factors-autophagy-and-apoptosis-in-mouse-macrophage-through-the-ros-signaling-pathway
#7
Tiansen Li, Yafang Xu, Laizhen Liu, Meiling Huang, Zhen Wang, Zhixia Tong, Hui Zhang, Fei Guo, Chuangfu Chen
Brucellosis is a highly contagious zoonosis caused by Brucella. Brucella can invade and persist inside host cells, which results in chronic infection. We constructed AIR interference and overexpression lentiviruses to acquire AIR interference, overexpression, and rescue stable expression cell lines. We also established a Brucella melitensis 16M-infected macrophage model, which was treated with either the vehicle control or NAC (ROS scavenger N-acetylcysteine (NAC) for 0, 3, 6, 12, and 24 h. Confocal laser microscopy, transmission electron microscopy, fluorescence quantitative PCR, flow cytometry, ELISA, and Western blot were used to detect inflammation, cell autophagy and apoptosis-related protein expression levels, ROS levels, and the distribution of mitochondria...
2016: PloS One
https://www.readbyqxmd.com/read/27903607/mitochondrial-division-occurs-concurrently-with-autophagosome-formation-but-independently-of-drp1-during-mitophagy
#8
Shun-Ichi Yamashita, Xiulian Jin, Kentaro Furukawa, Maho Hamasaki, Akiko Nezu, Hidenori Otera, Tetsu Saigusa, Tamotsu Yoshimori, Yasuyoshi Sakai, Katsuyoshi Mihara, Tomotake Kanki
Mitophagy is thought to play an important role in mitochondrial quality control. Mitochondrial division is believed to occur first, and autophagosome formation subsequently occurs to enwrap mitochondria as a process of mitophagy. However, there has not been any temporal analysis of mitochondrial division and autophagosome formation in mitophagy. Therefore, the relationships among these processes remain unclear. We show that the mitochondrial division factor Dnm1 in yeast or Drp1 in mammalian cells is dispensable for mitophagy...
December 5, 2016: Journal of Cell Biology
https://www.readbyqxmd.com/read/27903605/a-dividing-matter-drp1-dnm1-independent-mitophagy
#9
Martin Graef
Whether or not mitophagy depends on prior mitochondrial fragmentation by the canonical mitochondrial division machinery is controversial. In this issue, Yamashita et al. (2016. J. Cell Biol. https://doi.org/10.1083/jcb.201605093) report that mitochondrial fragments start to bud and divide from mitochondrial tubules when in tight association with forming autophagosomes, but independently of the mitochondrial division factor Drp1/Dnm1.
December 5, 2016: Journal of Cell Biology
https://www.readbyqxmd.com/read/27901103/fsh-protects-mouse-granulosa-cells-from-oxidative-damage-by-repressing-mitophagy
#10
Ming Shen, Yi Jiang, Zhiqiang Guan, Yan Cao, Shao-Chen Sun, Honglin Liu
Oxidative stress has been implicated in triggering granulosa cell (GC) death during follicular atresia. Recent studies suggested that follicle-stimulating hormone (FSH) has a pivotal role in protecting GCs from oxidative injury, although the exact mechanism remains largely unknown. Here, we report that FSH promotes GC survival by inhibiting oxidative stress-induced mitophagy. The loss of GC viability caused by oxidative stress was significantly reduced after FSH treatment, which was correlated with impaired activation of mitophagy upon oxidative stress...
November 30, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27881606/mitochondria-protection-after-acute-ischemia-prevents-prolonged-upregulation-of-il-1%C3%AE-and-il-18-and-arrests-ckd
#11
Hazel H Szeto, Shaoyi Liu, Yi Soong, Surya V Seshan, Leona Cohen-Gould, Viacheslav Manichev, Leonard C Feldman, Torgny Gustafsson
The innate immune system has been implicated in both AKI and CKD. Damaged mitochondria release danger molecules, such as reactive oxygen species, DNA, and cardiolipin, which can cause NLRP3 inflammasome activation and upregulation of IL-18 and IL-1β It is not known if mitochondrial damage persists long after ischemia to sustain chronic inflammasome activation. We conducted a 9-month study in Sprague-Dawley rats after 45 minutes of bilateral renal ischemia. We detected glomerular and peritubular capillary rarefaction, macrophage infiltration, and fibrosis at 1 month...
November 23, 2016: Journal of the American Society of Nephrology: JASN
https://www.readbyqxmd.com/read/27867381/a-critical-reappraisal-of-neutrophil-extracellular-traps-and-netosis-mimics-based-on-differential-requirements-for-protein-citrullination
#12
Maximilian F Konig, Felipe Andrade
NETosis, an antimicrobial form of neutrophil cell death, is considered a primary source of citrullinated autoantigens in rheumatoid arthritis (RA) and immunogenic DNA in systemic lupus erythematosus (SLE). Activation of the citrullinating enzyme peptidylarginine deiminase type 4 (PAD4) is believed to be essential for neutrophil extracellular trap (NET) formation and NETosis. PAD4 is therefore viewed as a promising therapeutic target to inhibit the formation of NETs in both diseases. In this review, we examine the evidence for PAD4 activation during NETosis and provide experimental data to suggest that protein citrullination is not a universal feature of NETs...
2016: Frontiers in Immunology
https://www.readbyqxmd.com/read/27864321/atg8-family-lc3-gabarap-proteins-are-crucial-for-autophagosome-lysosome-fusion-but-not-autophagosome-formation-during-pink1-parkin-mitophagy-and-starvation
#13
Thanh Ngoc Nguyen, Benjamin Scott Padman, Joanne Usher, Viola Oorschot, Georg Ramm, Michael Lazarou
Members of the Atg8 family of proteins are conjugated to autophagosomal membranes, where they have been proposed to drive autophagosome formation and selective sequestration of cargo. In mammals, the Atg8 family consists of six members divided into the LC3 and GABARAP subfamilies. To define Atg8 function, we used genome editing to generate knockouts of the LC3 and GABARAP subfamilies as well as all six Atg8 family members in HeLa cells. We show that Atg8s are dispensable for autophagosome formation and selective engulfment of mitochondria, but essential for autophagosome-lysosome fusion...
November 18, 2016: Journal of Cell Biology
https://www.readbyqxmd.com/read/27862231/early-stage-functions-of-mitochondrial-autophagy-and-oxidative-stress-in-acetaminophen-induced-liver-injury
#14
Yan Gao, Shifeng Chu, Zhao Zhang, Wei Zuo, Congyuan Xia, Qidi Ai, Piao Luo, Peng Cao, Naihong Chen
Mitochondria go through frequent cycles of fusion and fission, a process required for mitochondrial quality control by eliminating ROS-damaged mitochondria through mitochondrial autophagy. Acetaminophen (APAP) overdose can cause liver injury in animals and human beings by inducing mitochondrial damage, which need to be further evaluated. The aim of the current study is to assess the changes between oxidative damage and mitophagy in vivo and in vitro, which mimics APAP-induced liver injury (AILI) in humans. Liver damage was monitored by measuring the levels of biochemical indexes...
November 9, 2016: Journal of Cellular Biochemistry
https://www.readbyqxmd.com/read/27861891/opa1-haploinsufficiency-induces-a-bnip3-dependent-decrease-in-mitophagy-in-neurons-relevance-to-dominant-optic-atrophy
#15
Manon Moulis, Aurélie Millet, Marlène Daloyau, Marie-Christine Miquel, Brice Ronsin, Bernd Wissinger, Laetitia Arnauné-Pelloquin, Pascale Belenguer
Dominant Optic Atrophy (DOA) is due to mutations in the mitochondrial protein OPA1. The disease principally affects retinal ganglion cells, whose axons degenerate leading to vision impairments, and sometimes other neuronal phenotypes. The exact mechanisms underlying DOA pathogenesis are not known. We previously demonstrated that the main role of OPA1, as a mitochondrial fusogenic and anti-apoptotic protein, are inhibited by interaction with the stress inducible pro-apoptotic BNIP3 protein. Because BNIP3 was recently reported to participate in autophagy and mitophagy, we tested the involvement of these processes in DOA pathogenesis...
November 10, 2016: Journal of Neurochemistry
https://www.readbyqxmd.com/read/27861739/afzelin-ameliorates-d-galactosamine-and-lipopolysaccharide-induced-fulminant-hepatic-failure-by-modulating-mitochondrial-quality-control-and-dynamics-150-150
#16
Sang-Bin Lee, Jung-Woo Kang, So-Jin Kim, Jongmin Ahn, Jinwoong Kim, Sun-Mee Lee
BACKGROUND AND PURPOSE: Fulminant hepatic failure (FHF) is a fatal clinical syndrome that results in excessive inflammation and hepatocyte death. Mitochondrial dysfunction is considered to be a possible mechanism of FHF. Afzelin, a flavonol glycoside found in Houttuynia cordata Thunberg, has anti-inflammatory and antioxidant properties. The present study elucidated the cytoprotective mechanisms of afzelin against D-galactosamine (GalN)/lipopolysaccharide (LPS)-induced FHF, particularly focusing on mitochondrial quality control and dynamics...
November 15, 2016: British Journal of Pharmacology
https://www.readbyqxmd.com/read/27855364/parthenolide-induces-reactive-oxygen-species-mediated-autophagic-cell-death-in-human-osteosarcoma-cells
#17
Chen Yang, Qing Ou Yang, Qing-Jie Kong, Wen Yuan, Yue-Ping Ou Yang
BACKGROUND AND AIM: Osteosarcoma is a devastating tumor of bone, primarily affecting adolescents. Parthenolide, a naturally occurring small molecule that interferes with NF-κB signaling, has recently attracted considerable attention because of its pharmacological action involving anti-cancer effects. However, the mechanism of the cytotoxic effect exerted by parthenolide on tumor cells is not clearly defined today. METHODS: In this study, the effects of parthenolide were evaluated and characterized in human osteosarcoma cancer cell...
2016: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/27854125/apelin-apj-system-a-novel-therapeutic-target-for-myocardial-ischemia-reperfusion-injury
#18
Zhe Chen, Di Wu, Lanfang Li, Linxi Chen
Apelin is the endogenous ligand of the G protein-coupled receptor, APJ. Recently, researches indicate that the apelin/APJ system involves in myocardial ischemia-reperfusion injury (MIRI), which is a common pathophysiological process in patients with heart diseases and therapies. The reperfusion induces the expression of apelin and APJ receptor, which play an important role in cardioprotection of MIRI. The apelin/APJ system alleviates MIRI mainly by decreasing mitochondrial reactive oxygen species and delaying the opening of mitochondrial permeability transition pores, which induce the initiation of mitophagy...
November 17, 2016: DNA and Cell Biology
https://www.readbyqxmd.com/read/27853755/differential-stress-response-mechanisms-in-right-and-left-ventricles
#19
Makhosazane Zungu-Edmondson, Yuichiro J Suzuki
Right ventricular (RV) failure is the major cause of death among patients with pulmonary hypertension. However, differences between the RV and left ventricle (LV) of the adult heart have not been defined, despite myocytes from these two ventricles originate from different progenitor cells. The lack of such knowledge interferes with developing therapeutic strategies to protect the RV. The goal of this study was to identify possible differences between stress responses in the RV and LV free walls of adult rats...
2016: Journal of Rare Diseases Research & Treatment
https://www.readbyqxmd.com/read/27853101/trifloxystrobin-induced-mitophagy-through-mitochondrial-damage-in-human-skin-keratinocytes
#20
Yoonjeong Jang, Ji-Eun Kim, Sang-Hee Jeong, Min-Kyoung Paik, Jun Sung Kim, Myung-Haing Cho
Trifloxystrobin is a strobilurin class fungicide, the mode of action of which is to block the mitochondrial electron transport chain and inhibit energy production in fungi. Although adverse effects have been reported by occupational or environmental exposure of fungicides, the pathophysiological mechanism in human cells remains poorly understood. In the present study, we investigated the impact of trifloxystrobin on exposed skin at the cellular organelle level using HaCaT, the human skin keratinocyte cell line...
2016: Journal of Toxicological Sciences
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