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https://www.readbyqxmd.com/read/29665074/parkin-deficiency-modulates-nlrp3-inflammasome-activation-by-attenuating-an-a20-dependent-negative-feedback-loop
#1
François Mouton-Liger, Thibault Rosazza, Julia Sepulveda-Diaz, Amélie Ieang, Sidi-Mohamed Hassoun, Emilie Claire, Graziella Mangone, Alexis Brice, Patrick P Michel, Jean-Christophe Corvol, Olga Corti
Neuroinflammation and mitochondrial dysfunction, key mechanisms in the pathogenesis of Parkinson's disease (PD), are usually explored independently. Loss-of-function mutations of PARK2 and PARK6, encoding the E3 ubiquitin protein ligase Parkin and the mitochondrial serine/threonine kinase PINK1, account for a large proportion of cases of autosomal recessive early-onset PD. PINK1 and Parkin regulate mitochondrial quality control and have been linked to the modulation of innate immunity pathways. We report here an exacerbation of NLRP3 inflammasome activation by specific inducers in microglia and bone marrow-derived macrophages from Park2-/- and Pink1-/- mice...
April 17, 2018: Glia
https://www.readbyqxmd.com/read/29660402/lead-pb-induced-atm-dependent-mitophagy-via-pink1-parkin-pathway
#2
Xueyan Gu, Yongmei Qi, Zengxiu Feng, Lin Ma, Ke Gao, Yingmei Zhang
Lead (Pb), a widely distributed environmental pollutant, is known to induce mitochondrial damage as well as autophagy in vitro and in vivo. In this study, we found that Pb could trigger mitophagy in both HEK293 cells and the kidney cortex of male Kunming mice. However, whether ataxia telangiectasis mutated (ATM) which is reported to be linked with PTEN-induced putative kinase 1 (PINK1)/Parkin pathway (a well-characterized mitophagic pathway) participates in the regulation of Pb-induced mitophagy and its exact role remains enigmatic...
April 13, 2018: Toxicology Letters
https://www.readbyqxmd.com/read/29660306/ablation-of-toll-like-receptor-4-attenuates-aging-induced-myocardial-remodeling-and-contractile-dysfunction-through-ncori-hdac1-mediated-regulation-of-autophagy
#3
Shuyi Wang, Wei Ge, Carrie Harns, Xianzhong Meng, Yingmei Zhang, Jun Ren
Aging is usually accompanied with overt structural and functional changes as well as suppressed autophagy in the heart although the precise regulatory mechanisms are somewhat unknown. Here we evaluated the role of the innate proinflammatory mediator toll-like receptor 4 (TLR4) in cardiac aging and the underlying mechanism with a focus on autophagy. Cardiac geometry and function were monitored in young or old wild-type (WT) and TLR4 knockout (TLR4-/- ) mice using echocardiography, IonOptix® edge-detection and fura-2 techniques...
April 13, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29656925/dynamics-of-parkin-dependent-mitochondrial-ubiquitylation-in-induced-neurons-and-model-systems-revealed-by-digital-snapshot-proteomics
#4
Alban Ordureau, Joao A Paulo, Wei Zhang, Tim Ahfeldt, Jiuchun Zhang, Erin F Cohn, Zhonggang Hou, Jin-Mi Heo, Lee L Rubin, Sachdev S Sidhu, Steven P Gygi, J Wade Harper
Flux through kinase and ubiquitin-driven signaling systems depends on the modification kinetics, stoichiometry, primary site specificity, and target abundance within the pathway, yet we rarely understand these parameters and their spatial organization within cells. Here we develop temporal digital snapshots of ubiquitin signaling on the mitochondrial outer membrane in embryonic stem cell-derived neurons, and we model HeLa cell systems upon activation of the PINK1 kinase and PARKIN ubiquitin ligase by proteomic counting of ubiquitylation and phosphorylation events...
April 11, 2018: Molecular Cell
https://www.readbyqxmd.com/read/29655942/pink1-p-k520rfsx3-mutation-identified-in-a-chinese-family-with-early-onset-parkinson-s-disease
#5
Peng Wang, Yi Guo, Chengyuan Song, Yiming Liu, Hao Deng
Parkinson's disease (PD) features selective loss of dopaminergic neurons of the substantia nigra pars compacta accompanied by the accumulation and aggregation of alpha-synuclein in Lewy bodies. PTEN induced putative kinase 1 gene (PINK1) mutations are the second most common genetic cause of autosomal recessive early-onset Parkinson's disease (EOPD). A single nucleotide deletion in PINK1 exon 8 (c.1557delG) was identified in a consanguineous Chinese family with EOPD. The homozygous deletion was co-segregated with disease in the family and resulted in a frameshift after codon 520 with a premature termination at codon 522 (p...
April 12, 2018: Neuroscience Letters
https://www.readbyqxmd.com/read/29650039/carbon-black-suppresses-the-osteogenesis-of-mesenchymal-stem-cells-the-role-of-mitochondria
#6
Yulai Shen, Lu Wu, Dongdong Qin, Yankai Xia, Zhu Zhou, Xuemei Zhang, Xin Wu
BACKGROUND: The rapid increase in carbon black poses threats to human health. We evaluated the effect of CB (Printex 90) on the osteogenesis of bone-marrow-derived mesenchymal stem cells (MSCs). Mitochondria play an important role in the osteogenesis of MSCs and are potential targets of nanomaterials, so we studied the role of mitochondria in the CB Printex 90-induced effects on osteogenesis. RESULTS: Low doses of Printex 90 (3 ng/mL and 30 ng/mL) that did not cause deleterious effects on MSCs' viability significantly inhibited osteogenesis of MSCs...
April 12, 2018: Particle and Fibre Toxicology
https://www.readbyqxmd.com/read/29644727/genotype-phenotype-relations-for-the-parkinson-s-disease-genes-parkin-pink1-dj1-mdsgene-systematic-review
#7
REVIEW
Meike Kasten, Corinna Hartmann, Jennie Hampf, Susen Schaake, Ana Westenberger, Eva-Juliane Vollstedt, Alexander Balck, Aloysius Domingo, Franca Vulinovic, Marija Dulovic, Ingo Zorn, Harutyun Madoev, Hanna Zehnle, Christina M Lembeck, Leopold Schawe, Jennifer Reginold, Jana Huang, Inke R König, Lars Bertram, Connie Marras, Katja Lohmann, Christina M Lill, Christine Klein
This first comprehensive MDSGene review is devoted to the 3 autosomal recessive Parkinson's disease forms: PARK-Parkin, PARK-PINK1, and PARK-DJ1. It followed MDSGene's standardized data extraction protocol and screened a total of 3652 citations and is based on fully curated phenotypic and genotypic data on >1100 patients with recessively inherited PD because of 221 different disease-causing mutations in Parkin, PINK1, or DJ1. All these data are also available in an easily searchable online database (www...
April 11, 2018: Movement Disorders: Official Journal of the Movement Disorder Society
https://www.readbyqxmd.com/read/29642727/lps-challenge-increased-intestinal-permeability-disrupted-mitochondrial-function-and-triggered-mitophagy-of-piglets
#8
Shuting Cao, Qianhui Zhang, ChunChun Wang, Huan Wu, Lefei Jiao, Qihua Hong, Caihong Hu
Here we investigated the influence of LPS-induced gut injury on antioxidant homeostasis, mitochondrial (mt) function and the level of mitophagy in piglets. The results showed that LPS-induced intestinal injury decreased the transepithelial electrical resistance, increased the paracellular permeability of F1TC dextran 4 kDa, and decreased the expression of claudin-1, occludin and zonula occludens-1 in the jejunum compared with the control group. LPS decreased the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), and increased the content of malondialdehyde in the jejunum...
January 1, 2018: Innate Immunity
https://www.readbyqxmd.com/read/29626647/multiple-pathways-for-mitophagy-a-neurodegenerative-conundrum-for-parkinson-s-disease
#9
REVIEW
Charleen T Chu
It has been nearly a decade since the first landmark studies implicating familial recessive Parkinson's disease genes in the regulation of selective mitochondrial autophagy. The PTEN-induced kinase 1 (PINK1) and the E3 ubiquitin ligase Parkin (encoded by the PARK2 gene) act together to mark depolarized mitochondria for degradation. There is now an extensive body of literature detailing key mediators and steps in this pathway, based mostly on work in transformed cell lines. However, the degree to which PINK1-triggered mitophagy contributes to mitochondrial quality control in the mammalian brain, and the extent to which its disruption contributes to Parkinson's disease pathogenesis remain uncertain...
April 4, 2018: Neuroscience Letters
https://www.readbyqxmd.com/read/29617867/weaning-disrupts-intestinal-antioxidant-status-impairs-intestinal-barrier-and-mitochondrial-function-and-triggers-mitophagy-in-piglets
#10
S T Cao, C C Wang, H Wu, Q H Zhang, L F Jiao, C H Hu
In the present study, we investigated the influence of weaning on antioxidant status, intestinal integrity, mitochondrial function, and the mitophagy level in piglets (weaned at 21 d) during the 1 wk after weaning. The redox status was measured by antioxidant enzymes activities, related genes expression, and malondialdehyde (MDA) content in jejunum. The intestinal barrier function was assessed by the Ussing chamber and expression of tight junction proteins in the jejunum. The function of intestine mitochondria was measured by mitochondrial DNA (mtDNA) content and activities of mitochondria oxidative phosphorylation complexes...
April 3, 2018: Journal of Animal Science
https://www.readbyqxmd.com/read/29604498/oxidative-stress-and-mitochondrial-dysfunction-mediated-cd-induced-hepatic-lipid-accumulation-in-zebrafish-danio-rerio
#11
Ya-Xiong Pan, Zhi Luo, Mei-Qing Zhuo, Chuan-Chuan Wei, Guang-Hui Chen, Yu-Feng Song
The present study was performed to determine the effect of waterborne CdCl2 exposure influencing lipid deposition and metabolism, oxidative stress and mitochondrial dysfunction, and explore the underlying molecular mechanism of cadmium (Cd)-induced disorder of hepatic lipid metabolism in fish. To this end, adult zebrafish were exposed to three waterborne CdCl2 concentrations (0(control), 5 and 25 μg Cd/l, respectively) for 30 days. Lipid accumulation, the activities of enzymes related to lipid metabolism and oxidative stress, as well as the expression level of genes involved in lipid metabolism and mitophagy were determined in the liver of zebrafish...
March 17, 2018: Aquatic Toxicology
https://www.readbyqxmd.com/read/29603107/low-level-laser-irradiation-at-a-high-power-intensity-increased-human-endothelial-cell-exosome-secretion-via-wnt-signaling
#12
Hesam Saghaei Bagheri, Monireh Mousavi, Aysa Rezabakhsh, Jafar Rezaie, Seyed Hossein Rasta, Alireza Nourazarian, Çigir Biray Avci, Habib Tajalli, Mehdi Talebi, Ahmad Oryan, Majid Khaksar, Masoumeh Kazemi, Seyed Mahdi Nassiri, Shahrooz Ghaderi, Bakiye Goker Bagca, Reza Rahbarghazi, Emel Sokullu
The distinct role of low-level laser irradiation (LLLI) on endothelial exosome biogenesis remains unclear. We hypothesize that laser irradiation of high dose in human endothelial cells (ECs) contributes to the modulation of exosome biogenesis via Wnt signaling pathway. When human ECs were treated with LLLI at a power density of 80 J/cm2 , the survival rate reduced. The potential of irradiated cells to release exosomes was increased significantly by expressing genes CD63, Alix, Rab27a, and b. This occurrence coincided with an enhanced acetylcholine esterase activity, pseudopodia formation, and reduced zeta potential value 24 h post-irradiation...
March 30, 2018: Lasers in Medical Science
https://www.readbyqxmd.com/read/29589382/the-phosphodiesterase-4-inhibitor-roflumilast-protects-against-cigarette-smoke-extract-induced-mitophagy-dependent-cell-death-in-epithelial-cells
#13
Sun Young Kyung, Yu Jin Kim, Eun Suk Son, Sung Hwan Jeong, Jeong Woong Park
BACKGROUND: Recent studies show that mitophagy, the autophagy-dependent turnover of mitochondria, mediates pulmonary epithelial cell death in response to cigarette smoke extract (CSE) exposure and contributes to the development of emphysema in vivo during chronic cigarette smoke (CS) exposure, although the underlying mechanisms remain unclear. METHODS: In this study, we investigated the role of mitophagy in the regulation of CSE-exposed lung bronchial epithelial cell (Beas-2B) death...
April 2018: Tuberculosis and Respiratory Diseases
https://www.readbyqxmd.com/read/29567065/pink1-parkin-mediated-mitophagy-was-activated-against-1-4-enzoquinone-induced-apoptosis-in-hl-60-cells
#14
Chunxiao Zhang, Xiuyuan Yu, Jiahao Gao, Qianqian Zhang, Shuqiang Sun, Hua Zhu, Xinjun Yang, Hongtao Yan
Hematotoxicity of benzene is derived mainly from its active metabolite, 1,4-Benzoquinone (1,4-BQ), which induces cell apoptosis and mitochondrial damage. Damaged mitochondria are degraded through a specialized autophagy pathway, called mitophagy, which is driven by PINK1/Parkin signaling. However, whether mitophagy is involved in 1,4-BQ-induced toxicity remains unclear. This study was designed to investigate whether PINK1/Parkin-mediated mitophagy is activated in 1,4-BQ-treated HL-60 cells, and the roles mitophagy plays in 1,4-BQ-induced apoptosis...
March 19, 2018: Toxicology in Vitro: An International Journal Published in Association with BIBRA
https://www.readbyqxmd.com/read/29563990/insulin-alleviates-mitochondrial-oxidative-stress-involving-upregulation-of-superoxide-dismutase-2-and-uncoupling-protein-2-in-septic-acute-kidney-injury
#15
Guang-Dao Chen, Jun-Liang Zhang, Yi-Ting Chen, Ju-Xing Zhang, Tao Wang, Qi-Yi Zeng
The aim of the present study was to explore the effects and mechanisms of insulin on mitochondrial oxidative stress in septic acute kidney injury (AKI). Male Sprague Dawley rats were divided randomly into four groups: Control group, sham surgery group, cecal ligation and puncture (CLP) group, and CLP plus insulin group. Blood specimens and kidney tissues were obtained at 12 and 24 h after surgery as separate experiments. Analyses of histology and indicators of renal injury [blood urea nitrogen (BUN) and serum creatinine (CRE) and neutrophil gelatinase-associated lipocalin (NGAL)], mitochondrial function [adenosine triphosphate (ATP) and mitochondrial membrane potential (MMP)], oxidative stress [inducible nitric oxide synthase (iNOS), reactive oxygen species (ROS) and nitric oxide (NO)], endogenous antioxidant systems [superoxide dismutase (SOD) and glutathione (GSH)] as well as the expression of uncoupling protein (UCP), PINK1 protein (a major mediator of mitophagy), PGC1α protein (a major regulator of mitochondrial biogenesis) were performed...
April 2018: Experimental and Therapeutic Medicine
https://www.readbyqxmd.com/read/29563254/phosphorylation-of-mcad-selectively-rescues-pink1-deficiencies-in-behavior-and-metabolism
#16
Meredith M Course, Anna I Scott, Carmen Schoor, Chung-Han Hsieh, Amanda M Papakyrikos, Dominic Winter, Tina M Cowan, Xinnan Wang
PINK1 is a mitochondria-targeted kinase, whose mutations are a cause of Parkinson's disease. We set out to better understand PINK1's effects on mitochondrial proteins in vivo Using an unbiased phosphoproteomic screen in Drosophila , we found that PINK1 mediates the phosphorylation of MCAD, a mitochondrial matrix protein critical to fatty acid metabolism. By mimicking phosphorylation of this protein in a PINK1 null background, we restored PINK1 null's climbing, flight, thorax, and wing deficiencies. Due to MCAD's role in fatty acid metabolism, we examined the metabolic profile of PINK1 null flies, where we uncovered significant disruptions in both acylcarnitines and amino acids...
March 21, 2018: Molecular Biology of the Cell
https://www.readbyqxmd.com/read/29562342/diquat-induced-oxidative-stress-increases-intestinal-permeability-impairs-mitochondrial-function-and-triggers-mitophagy-in-piglets
#17
Shuting Cao, Huan Wu, ChunChun Wang, Qianhui Zhang, Lefei Jiao, Fanghui Lin, Caihong Hu
In the present study, we investigated the influence of diquat-induced oxidative stress on intestinal barrier, mitochondrial function and the level of mitophagy in piglets. Twelve male Duroc×Landrace×Yorkshire 35-d-old pigs (weaned at 21d of age), with an average body of 9.6 kg, were allotted to two treatments of six piglets each including the challenged group and the control group. The challenged pigs were injected with 100 mg/kg bodyweight diquat and control pigs injected with 0.9% (w/v) NaCl solution. The results showed that diquat injection decreased average daily feed intake and average daily gain...
March 17, 2018: Journal of Animal Science
https://www.readbyqxmd.com/read/29561660/loss-of-parkin-impairs-mitochondrial-function-and-leads-to-muscle-atrophy
#18
Nesibe Peker, Vinay Donipadi, Mridula Sharma, Craig McFarlane, Ravi Kambadur
Parkinson's Disease is a neurodegenerative disease characterized by tremors, muscle stiffness and muscle weakness. Molecular genetic analysis confirmed that mutations in PARKIN and PINK1 genes, which play major roles in mitochondrial quality control and mitophagy, are frequently associated with Parkinson's Disease. PARKIN is an E3 ubiquitin ligase that translocates to mitochondria during loss of mitochondrial membrane potential to increase mitophagy. Although muscle dysfunction is noted in Parkinson's Disease, little is known about the involvement of PARKIN in the muscle phenotype of Parkinson's Disease...
March 21, 2018: American Journal of Physiology. Cell Physiology
https://www.readbyqxmd.com/read/29560088/mitochondrial-quality-control-beyond-pink1-parkin
#19
EDITORIAL
Sophia von Stockum, Elena Marchesan, Elena Ziviani
No abstract text is available yet for this article.
February 27, 2018: Oncotarget
https://www.readbyqxmd.com/read/29530980/impact-of-altered-phosphorylation-on-loss-of-function-of-juvenile-parkinsonism-associated-genetic-variants-of-the-e3-ligase-parkin
#20
Jacob D Aguirre, Karen M Dunkerley, Rica Lam, Michele Rusal, Gary S Shaw
Autosomal recessive juvenile Parkinsonism (ARJP) is an inherited neurodegenerative disease in which 50% of affected individuals harbor mutations in the gene encoding the E3 ligase parkin. Parkin regulates the mitochondrial recycling pathway, which is induced by oxidative stress. In its native state, parkin is autoinhibited by its N-terminal ubiquitin-like (Ubl) domain which blocks the binding site for an incoming E2~ubiquitin conjugate, needed for parkin's ubiquitination activity. Parkin is activated via phosphorylation of Ser65 in its Ubl domain by PTEN-induced putative kinase 1 (PINK1) and an ubiquitin molecule phosphorylated at a position equivalent to Ser65 in parkin...
March 12, 2018: Journal of Biological Chemistry
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