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https://www.readbyqxmd.com/read/28324645/three-dimensional-analysis-of-somatic-mitochondrial-dynamics-in-fission-deficient-injured-motor-neurons-using-fib-sem
#1
Hiromi Tamada, Sumiko Kiryu-Seo, Hiroki Hosokawa, Keisuke Ohta, Naotada Ishihara, Masatoshi Nomura, Katsuyoshi Mihara, Kei-Ichiro Nakamura, Hiroshi Kiyama
Mitochondria undergo morphological changes through fusion and fission for their quality control, which are vital for neuronal function. In this study, we examined three-dimensional morphologies of mitochondria in motor neurons under normal, nerve injured, and nerve injured plus fission-impaired conditions using the focused ion beam/scanning electron microscopy (FIB/SEM), because the FIB/SEM technology is a powerful tool to demonstrate both 3D images of whole organelle and the intra-organellar structure simultaneously...
March 21, 2017: Journal of Comparative Neurology
https://www.readbyqxmd.com/read/28324492/detection-of-hypoxia-induced-and-iron-depletion-induced-mitophagy-in-mammalian-cells
#2
Shun-Ichi Yamashita, Tomotake Kanki
Mitochondrial quality and quantity are not only regulated by mitochondrial fusion and fission but also by mitochondria degradation. Mitophagy, an autophagy specific for damaged or unnecessary mitochondria, is believed to be an important pathway for mitochondrial homeostasis. To date, several stimuli are known to induce mitophagy. Some of these stimuli, however, including hypoxia, iron depletion, and nitrogen starvation, induce mild mitophagy, which is difficult to detect through decreased mitochondrial mass...
March 22, 2017: Methods in Molecular Biology
https://www.readbyqxmd.com/read/28324491/monitoring-mitophagy-during-aging-in-caenorhabditis-elegans
#3
Nikolaos Charmpilas, Konstantinos Kounakis, Nektarios Tavernarakis
Mitochondria constitute the main energy-producing centers of eukaryotic cells. In addition, they are involved in several crucial cellular processes, such as lipid metabolism, calcium buffering, and apoptosis. As such, their malfunction can be detrimental for proper cellular physiology and homeostasis. Mitophagy is a mechanism that protects and maintains cellular function by sequestering harmful or dysfunctional mitochondria to lysosomes for degradation. In this report, we present experimental procedures for quantitative, in vivo monitoring of mitophagy events in the nematode Caenorhabditis elegans...
March 22, 2017: Methods in Molecular Biology
https://www.readbyqxmd.com/read/28324490/assessment-of-mitophagy-in-ips-cell-derived-neurons
#4
Kei-Ichi Ishikawa, Akihiro Yamaguchi, Hideyuki Okano, Wado Akamatsu
Aberrant mitochondrial function is associated with many neurological diseases. Mitophagy is a key mechanism for the elimination of damaged mitochondria and maintenance of mitochondrial homeostasis. Induced pluripotent stem (iPS) cell technologies developed over the last decade have allowed us to analyze functions of the human neuron. Here we describe an efficient induction method from human iPS cells to neurons, followed by an image-based mitophagy assay.
March 22, 2017: Methods in Molecular Biology
https://www.readbyqxmd.com/read/28324489/monitoring-mitochondrial-changes-by-alteration-of-the-pink1-parkin-signaling-in-drosophila
#5
Tsuyoshi Inoshita, Kahori Shiba-Fukushima, Hongrui Meng, Nobutaka Hattori, Yuzuru Imai
Mitochondrial quality control is a key process in tissues with high energy demands, such as the brain and muscles. Recent studies using Drosophila have revealed that the genes responsible for familial forms of juvenile Parkinson's disease (PD), PINK1 and Parkin regulate mitochondrial function and motility. Cell biological analysis using mammalian cultured cells suggests that the dysregulation of mitophagy by PINK1 and Parkin leads to neurodegeneration in PD. In this chapter, we describe the methods to monitor mitochondrial morphology in the indirect flight muscles of adult Drosophila and Drosophila primary cultured neurons and the methods to analyze the motility of mitochondria in the axonal transport of living larval motor neurons...
March 22, 2017: Methods in Molecular Biology
https://www.readbyqxmd.com/read/28324488/flow-cytometer-monitoring-of-bnip3-and-bnip3l-nix-dependent-mitophagy
#6
Matilda Šprung, Ivan Dikic, Ivana Novak
Mitochondria are organelles with numerous vital roles in cellular metabolism. Impaired or damaged mitochondria are degraded in autophagolysosomes in a process known as mitophagy. Given the fundamental role of mitophagy in maintenance of cellular homeostasis, methods and techniques with which to study this process are constantly evolving and emerging. So far, mitophagy flux was mostly monitored using fluorescently labeled LC3 protein on autophagosomal membrane and any of the labeled outer mitochondrial membrane proteins...
March 22, 2017: Methods in Molecular Biology
https://www.readbyqxmd.com/read/28324487/mitophagy-in-yeast-a-screen-of-mitophagy-deficient-mutants
#7
Kentaro Furukawa, Tomotake Kanki
Mitochondrial autophagy (mitophagy) is a process that selectively degrades mitochondria via autophagy. Recent studies have shown that mitophagy plays an important role in mitochondrial homeostasis by degrading damaged or excess mitochondria. The budding yeast Saccharomyces cerevisiae is a powerful model organism that has been employed to study several biological phenomena. Recently, there has been significant progress in the understanding of mitophagy in yeast following the identification of Atg32, a mitochondrial outer membrane receptor protein for mitophagy...
March 22, 2017: Methods in Molecular Biology
https://www.readbyqxmd.com/read/28324486/mitopho8%C3%AE-60-assay-as-a-tool-to-quantitatively-measure-mitophagy-activity
#8
Zhiyuan Yao, Xu Liu, Daniel J Klionsky
Mitophagy, a selective type of macroautophagy (hereafter referred to as autophagy), specifically mediates the vacuole/lysosome-dependent degradation of damaged or surplus mitochondria. Because this process regulates the number and quality of mitochondria, it is vital for proper cellular homeostasis. Mitophagy also plays critical roles in the clearance of paternal mitochondria in C. elegans embryos, in erythroid cell maturation, and in the prevention of neurodegenerative disease and cancer. In order to study the molecular mechanism and regulation of mitophagy, sensitive assays are necessary to quantitatively measure mitophagy activity...
March 22, 2017: Methods in Molecular Biology
https://www.readbyqxmd.com/read/28323531/mitophagy-receptor-fundc1-regulates-mitochondrial-homeostasis-and-protects-the-heart-from-i-r-injury
#9
Weilin Zhang, Sami Siraj, Rong Zhang, Quan Chen
Mitophagy plays pivotal roles in the selective disposal of unwanted mitochondria, and accumulation of damaged mitochondria has been linked to ageing-related diseases. However, definitive proof that mitophagy regulates mitochondrial quality in vivo is lacking. It is also largely unclear whether damaged mitochondria are the cause or just the consequence of these diseases. We previously showed that FUNDC1 is a mitophagy receptor that interacts with LC3 to mediate mitophagy in response to hypoxia in cultured cells...
March 21, 2017: Autophagy
https://www.readbyqxmd.com/read/28320180/mitochondrial-dysfunction-silent-killer-in-cerebral-ischemia
#10
REVIEW
Pramila Bakthavachalam, Prakash Srinivasan Timiri Shanmugam
Mitochondrial dysfunction aggravates ischemic neuronal injury through activation of various pathophysiological and molecular mechanisms. Ischemic neuronal injury is particularly intensified during reperfusion due to impairment of mitochondrial function. Mitochondrial mutilation instigates alterations in calcium homeostasis in neurons, which plays a pivotal role in the maintenance of normal neuronal function. Increase in intracellular calcium level in mitochondria triggers the opening of mitochondrial transition pore and over production of reactive oxygen species (ROS)...
April 15, 2017: Journal of the Neurological Sciences
https://www.readbyqxmd.com/read/28316186/-progresses-of-mitophagy-in-heart-disease
#11
P Yu, K Hong
No abstract text is available yet for this article.
March 24, 2017: Zhonghua Xin Xue Guan Bing za Zhi
https://www.readbyqxmd.com/read/28296541/pharmacological-modulators-of-autophagy-activate-a-parallel-noncanonical-pathway-driving-unconventional-lc3-lipidation
#12
Elise Jacquin, Stéphanie Leclerc-Mercier, Celine Judon, Emmanuelle Blanchard, Sylvie Fraitag, Oliver Florey
The modulation of canonical macroautophagy/autophagy for therapeutic benefit is an emerging strategy of medical and pharmaceutical interest. Many drugs act to inhibit autophagic flux by targeting lysosome function, while others were developed to activate the pathway. Here, we report the surprising finding that many therapeutically relevant autophagy modulators with lysosomotropic and ionophore properties, classified as inhibitors of canonical autophagy, are also capable of activating a parallel noncanonical autophagy pathway that drives MAP1LC3/LC3 lipidation on endolysosomal membranes...
February 15, 2017: Autophagy
https://www.readbyqxmd.com/read/28294175/the-age-associated-loss-of-ischemic-preconditioning-in-the-kidney-is-accompanied-by-mitochondrial-dysfunction-increased-protein-acetylation-and-decreased-autophagy
#13
Stanislovas S Jankauskas, Irina B Pevzner, Nadezda V Andrianova, Ljubava D Zorova, Vasily A Popkov, Denis N Silachev, Nataliya G Kolosova, Egor Y Plotnikov, Dmitry B Zorov
In young rats, ischemic preconditioning (IPC), which consists of 4 cycles of ischemia and reperfusion alleviated kidney injury caused by 40-min ischemia. However,old rats lost their ability to protect the ischemic kidney by IPC. A similar aged phenotype was demonstrated in 6-month-old OXYS rats having signs of premature aging. In the kidney of old and OXYS rats, the levels of acetylated nuclear proteins were higher than in young rats, however, unlike in young rats, acetylation levels in old and OXYS rats were further increased after IPC...
March 15, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28292026/catalpol-protects-glucose-deprived-rat-embryonic-cardiac-cells-by-inducing-mitophagy-and-modulating-estrogen-receptor
#14
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...
March 9, 2017: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/28288130/parl-mediates-smac-proteolytic-maturation-in-mitochondria-to-promote-apoptosis
#15
Shotaro Saita, Hendrik Nolte, Kai Uwe Fiedler, Hamid Kashkar, A Saskia Venne, René P Zahedi, Marcus Krüger, Thomas Langer
Mitochondria drive apoptosis by releasing pro-apoptotic proteins that promote caspase activation in the cytosol. The rhomboid protease PARL, an intramembrane cleaving peptidase in the inner membrane, regulates mitophagy and plays an ill-defined role in apoptosis. Here, we employed PARL-based proteomics to define its substrate spectrum. Our data identified the mitochondrial pro-apoptotic protein Smac (also known as DIABLO) as a PARL substrate. In apoptotic cells, Smac is released into the cytosol and promotes caspase activity by inhibiting inhibitors of apoptosis (IAPs)...
March 13, 2017: Nature Cell Biology
https://www.readbyqxmd.com/read/28281653/nix-restores-mitophagy-and-mitochondrial-function-to-protect-against-pink1-parkin-related-parkinson-s-disease
#16
Brianada Koentjoro, Jin-Sung Park, Carolyn M Sue
Therapeutic targets are needed to develop neuroprotective treatments for Parkinson's disease (PD). Mitophagy, the selective autophagic elimination of dysfunctional mitochondria, is essential for the maintenance of mitochondrial integrity and is predominantly regulated by the PINK1/Parkin-mediated pathway. Loss of function mutations in Parkin and PINK1 cause an accumulation of dysfunctional mitochondria, leading to nigral neurodegeneration and early-onset PD with a high penetrance rate. We previously identified an asymptomatic homozygous Parkin mutation carrier who had not developed PD by her eighth decade despite the loss of functional Parkin...
March 10, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28276439/structure-guided-mutagenesis-reveals-a-hierarchical-mechanism-of-parkin-activation
#17
Matthew Y Tang, Marta Vranas, Andrea I Krahn, Shayal Pundlik, Jean-François Trempe, Edward A Fon
Parkin and PINK1 function in a common pathway to clear damaged mitochondria. Parkin exists in an auto-inhibited conformation stabilized by multiple interdomain interactions. The binding of PINK1-generated phospho-ubiquitin and the phosphorylation of the ubiquitin-like (Ubl) domain of Parkin at Ser65 release its auto-inhibition, but how and when these events take place in cells remain to be defined. Here we show that mutations that we designed to activate Parkin by releasing the Repressor Element of Parkin (REP) domain, or by disrupting the interface between the RING0:RING2 domains, can completely rescue mutations in the Parkin Ubl that are defective in mitochondrial autophagy...
March 9, 2017: Nature Communications
https://www.readbyqxmd.com/read/28276029/assessing-mitochondrial-selective-autophagy-in-the-nematode-caenorhabditis-elegans
#18
Konstantinos Palikaras, Nektarios Tavernarakis
Eukaryotic cells heavily depend on ATP generated by oxidative phosphorylation (OXPHOS) within mitochondria. Besides being the main suppliers of cell's energy, mitochondria also provide an additional compartment for a wide range of cellular processes and metabolic pathways. Mitochondria constantly undergo fusion/fission events and form a mitochondrial network, which is a highly dynamic, tubular structure allowing for rapid and continuous exchange of genetic material, as well as, targeting dysfunctional mitochondria for degradation through mitochondrial selective autophagy (mitophagy)...
2017: Methods in Molecular Biology
https://www.readbyqxmd.com/read/28276028/assays-for-mitophagy-in-yeast
#19
Akinori Eiyama, Koji Okamoto
Elimination of damaged or surplus mitochondria is crucial to maintain cellular integrity and an energy supply-demand balance. Mitophagy serves to selectively catabolize mitochondria in a manner dependent on autophagy, and contributes to mitochondrial quality and quantity control. This degradation system is highly conserved among eukaryotes including the budding yeast, Saccharomyces cerevisiae. Therefore, analyses of mitophagy using yeast have the potential to provide insights into the common mechanisms of mitophagy...
2017: Methods in Molecular Biology
https://www.readbyqxmd.com/read/28272266/lack-of-activation-of-mitophagy-during-endurance-exercise-in-human
#20
Céline Schwalm, Louise Deldicque, Marc Francaux
PURPOSE: To determine whether fission and mitophagy are activated by acute endurance exercise in human skeletal muscle and to investigate if this activation is dependent upon the nutritional state. METHODS: Trained athletes (n = 7) cycled for 2 h at 70% VO2 peak in a fed or fasted state. Vastus lateralis muscle biopsies were obtained at baseline, before, immediately after and 1 h after exercise. Protein and mRNA markers for mitophagy, mitochondrial biogenesis, fission and fusion were analyzed using qRT-PCR and Western blot...
March 8, 2017: Medicine and Science in Sports and Exercise
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