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https://www.readbyqxmd.com/read/28527631/the-thiol-switch-c684-in-mitofusin-2-mediates-redox-induced-alterations-of-mitochondrial-shape-and-respiration
#1
Osamah Thaher, Christina Wolf, Partha Narayan Dey, Alireza Pouya, Verena Wüllner, Stefan Tenzer, Axel Methner
Mitofusin-2 (MFN2) is a GTPase in the outer mitochondrial membrane involved in the regulation of mitochondrial fusion and bioenergetics. MFN2 also plays a role in mitochondrial fusion induced by changes in the intracellular redox state. Adding oxidized glutathione (GSSG), the core cellular stress indicator, to mitochondrial preparations stimulates mitochondrial fusion by inducing disulphide bond-mediated oligomer formation of MFN2 and its homolog MFN1 which involve cysteine 684 (C684) of MFN2. Mitochondrial hyperfusion represents an adaptive stress response that confers transient protection by increasing mitochondrial ATP production but how this depends on the thiol switch C684 in MFN2 has not been investigated...
May 17, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28514731/antagonistic-effects-of-selenium-on-cadmium-induced-apoptosis-by-restoring-the-mitochondrial-dynamic-equilibrium-and-energy-metabolism-in-chicken-spleens
#2
Zhe Xu, Xi Jin, Tingru Pan, Tianqi Liu, Na Wan, Shu Li
The aim of this study was to investigate the mechanism of cadmium-induced apoptosis in chicken spleens and the antagonistic effects of selenium. We duplicated the selenium-cadmium interaction model and examined the expression of apoptosis-, immune-, mitochondrial dynamics- and energy metabolism-related genes. The results demonstrated that after treatment with cadmium, the frequency of apoptosis was significantly increased, and the morphological characteristics of apoptosis were observed. The expression of pro-apoptotic genes was increased, and that of anti-apoptotic genes was decreased...
April 30, 2017: Oncotarget
https://www.readbyqxmd.com/read/28513770/association-between-mfn2-gene-polymorphisms-and-the-risk-and-prognosis-of-acute-liver-failure-a-case-control-study-in-a-chinese-population
#3
Y-L Wei, Q Tian, X-X Zhao, G-Z Qiu, Y Xu
This study aimed to determine the role of mitofusin 2 (MFN2) gene polymorphisms in the risk and prognosis of acute liver failure (ALF). A total of 298 blood samples were collected from 138 ALF patients (case group) and 160 healthy participants (control group). Coagulation function, glutamic pyruvic transaminase (GPT), glutamic oxaloacetic transaminase (GOT), total bilirubin (TB), blood ammonia and lactic acid (LA) were measured. The predictive evaluation of MFN2 gene polymorphisms in the risk and prognosis of ALF patients was estimated using Kaplan-Meier survival analysis, haplotype analysis, binary logistic regression analysis and Cox regression analysis...
May 15, 2017: Brazilian Journal of Medical and Biological Research, Revista Brasileira de Pesquisas Médicas e Biológicas
https://www.readbyqxmd.com/read/28487236/upregulation-of-mir-195-accelerates-oxidative-stress-induced-retinal-endothelial-cell-injury-by-targeting-mitofusin-2-in-diabetic-rats
#4
Rui Zhang, Qian Garrett, Huimin Zhou, Xiaoxi Wu, Yueran Mao, Ximing Cui, Bing Xie, Zanchao Liu, Dongsheng Cui, Lei Jiang, Qingfu Zhang, Shunjiang Xu
This study was performed to investigate the oxidative stress-induced miRNA changes in relation to pathogenesis of diabetic retinopathy (DR) and to establish a functional link between miRNAs and oxidative stress-induced retinal endothelial cell injury. Our results demonstrated that oxidative stress could induce alterations of miRNA expression profile, including up-regulation of miR-195 in the diabetic retina or cultured HMRECs after exposed to H2O2 or HG (P < 0.05). Oxidative stress also resulted in a significant reduction of MFN2 expression in diabetic retina or HMRECs (P < 0...
May 6, 2017: Molecular and Cellular Endocrinology
https://www.readbyqxmd.com/read/28486121/mitochondrial-homeostasis-how-do-dimers-of-mitofusins-mediate-mitochondrial-fusion
#5
Oliver Daumke, Aurélien Roux
Mitochondria have high fusion and fission rates to maintain their size and number throughout the cell cycle. How is fusion mediated? New structural studies propose mechanisms by which the dynamin-like mitofusin proteins promote fusion of mitochondria.
May 8, 2017: Current Biology: CB
https://www.readbyqxmd.com/read/28483668/doxorubicin-induced-cardiomyocyte-apoptosis-role-of-mitofusin-2
#6
Han Tang, Aibin Tao, Jia Song, Qian Liu, Hao Wang, Tao Rui
BACKGROUND: Doxorubicin (DOX) is an anti-tumor agent that is widely used in clinical setting for cancer treatment. The application of the DOX, however, is limited by its cardiac toxicity which can induce heart failure through an undefined mechanism. Mitofusin 2 (Mfn2) is a mitochondrial GTPase fusion protein that is located on the outer membrane of mitochondria (OMM). The Mfn2 plays an important role in mitochondrial fusion and fission. The aim of this study is to identify the role of the Mfn2 in DOX-induced cardiomyocyte apoptosis...
May 5, 2017: International Journal of Biochemistry & Cell Biology
https://www.readbyqxmd.com/read/28483572/early-energy-metabolism-related-molecular-events-in-skeletal-muscle-of-diabetic-rats-the-effects-of-l-arginine-and-sod-mimic
#7
Ana Stancic, Milos Filipovic, Ivana Ivanovic-Burmazovic, Sava Masovic, Aleksandra Jankovic, Vesna Otasevic, Aleksandra Korac, Biljana Buzadzic, Bato Korac
Considering the vital role of skeletal muscle in control of whole-body metabolism and the severity of long-term diabetic complications, we aimed to reveal the molecular pattern of early diabetes-related skeletal muscle phenotype in terms of energy metabolism, focusing on regulatory mechanisms, and the possibility to improve it using two redox modulators, l-arginine and superoxide dismutase (SOD) mimic. Alloxan-induced diabetic rats (120 mg/kg) were treated with l-arginine or the highly specific SOD mimic, M40403, for 7 days...
May 5, 2017: Chemico-biological Interactions
https://www.readbyqxmd.com/read/28460043/cell-free-mitochondrial-fusion-assay-detected-by-specific-protease-reaction-revealed-ca2-as-regulator-of-mitofusin-dependent-mitochondrial-fusion
#8
Naotada Ishihara, Maki Maeda, Tadato Ban, Katsuyoshi Mihara
Mitochondrial dynamic by frequent fusion and fission have important roles in various cellular signaling processes and pathophysiology in vivo. However, the molecular mechanisms that regulate mitochondrial fusion, especially in mammalian cells, are not well understood. Accordingly, we developed a novel biochemical cell-free mitochondrial fusion assay system using isolated human mitochondria. We used a protease and its specific substrate that are essential for yeast autophagy; Atg4 protease is required for maturation and the de-conjugation of the ubiquitin-like modifier Atg8...
April 27, 2017: Journal of Biochemistry
https://www.readbyqxmd.com/read/28455958/csfv-induced-mitochondrial-fission-and-mitophagy-to-inhibit-apoptosis
#9
Hongchao Gou, Mingqiu Zhao, Hailuan Xu, Jin Yuan, Wencheng He, Mengjiao Zhu, Hongxing Ding, Lin Yi, Jinding Chen
Classical swine fever virus (CSFV), which causes typical clinical characteristics in piglets, including hemorrhagic syndrome and immunosuppression, is linked to hepatitis C and dengue virus. Oxidative stress and a reduced mitochondrial transmembrane potential are disturbed in CSFV-infected cells. The balance of mitochondrial dynamics is essential for cellular homeostasis. In this study, we offer the first evidence that CSFV induces mitochondrial fission and mitophagy to inhibit host cell apoptosis for persistent infection...
April 11, 2017: Oncotarget
https://www.readbyqxmd.com/read/28414270/human-biallelic-mfn2-mutations-induce-mitochondrial-dysfunction-upper-body-adipose-hyperplasia-and-suppression-of-leptin-expression
#10
Nuno Rocha, David A Bulger, Andrea Frontini, Hannah Titheradge, Sigrid Bjerge Gribsholt, Rachel Knox, Matthew Page, Julie Harris, Felicity Payne, Claire Adams, Alison Sleigh, John Crawford, Anette Prior Gjesing, Jette Bork-Jensen, Oluf Pedersen, Inês Barroso, Torben Hansen, Helen Cox, Mary Reilly, Alex Rossor, Rebecca J Brown, Simeon I Taylor, Duncan McHale, Martin Armstrong, Elif A Oral, Vladimir Saudek, Stephen O'Rahilly, Eamonn R Maher, Bjørn Richelsen, David B Savage, Robert K Semple
MFN2 encodes mitofusin 2, a membrane-bound mediator of mitochondrial membrane fusion and inter-organelle communication. MFN2 mutations cause axonal neuropathy, with associated lipodystrophy only occasionally noted, however homozygosity for the p.Arg707Trp mutation was recently associated with upper body adipose overgrowth. We describe similar massive adipose overgrowth with suppressed leptin expression in four further patients with biallelic MFN2 mutations and at least one p.Arg707Trp allele. Overgrown tissue was composed of normal-sized, UCP1-negative unilocular adipocytes, with mitochondrial network fragmentation, disorganised cristae, and increased autophagosomes...
April 19, 2017: ELife
https://www.readbyqxmd.com/read/28404953/hydrogen-rich-saline-attenuates-spinal-cord-hemisection-induced-testicular-injury-in-rats
#11
Li Ge, Li-Hua Wei, Chang-Qing Du, Guo-Hua Song, Ya-Zhuo Xue, Hao-Shen Shi, Ming Yang, Xin-Xin Yin, Run-Ting Li, Xue-Er Wang, Zhen Wang, Wen-Gang Song
To study how hydrogen-rich saline (HS) promotes the recovery of testicular biological function in a hemi-sectioned spinal cord injury (hSCI) rat model, a right hemisection was performed at the T11-T12 of the spinal cord in Wistar rats. Animals were divided into four groups: normal group; vehicle group: sham-operated rats administered saline; hSCI group: subjected to hSCI and administered saline; HRST group: subjected to hSCI and administered HS. Hind limb neurological function, testis index, testicular morphology, mean seminiferous tubular diameter (MSTD) and seminiferous epithelial thickness (MSET), the expression of heme oxygenase-1 (HO-1), mitofusin-2 (MFN-2), and high-mobility group box 1 (HMGB-1), cell ultrastructure, and apoptosis of spermatogenic cells were studied...
March 3, 2017: Oncotarget
https://www.readbyqxmd.com/read/28381463/chronic-kidney-disease-induces-autophagy-leading-to-dysfunction-of-mitochondria-in-skeletal-muscle
#12
Zhen Su, Janet D Klein, Jie DU, Harold A Franch, Liping Zhang, Faten Hassounah, Matthew B Hudson, Xiaonan H Wang
Chronic kidney disease (CKD) causes loss of lean body mass by multiple mechanisms. This study examines whether autophagy-mediated proteolysis contributes to CKD-induced muscle wasting. We tested autophagy in the muscle of CKD mice with plantaris muscle overloading to mimic resistance exercise or with acupuncture plus low frequency electrical stimulation (Acu/LFES) treatment. In CKD muscle, Bnip3, Beclin-1, LC3II mRNAs and proteins were increased compared with control muscle, indicating autophagosome-lysosome formation induction...
April 5, 2017: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/28380071/the-abundance-of-the-arl2-gtpase-and-its-gap-elmod2-at-mitochondria-are-modulated-by-the-fusogenic-activity-of-mitofusins-and-stressors
#13
Laura E Newman, Cara R Schiavon, Chengjing Zhou, Richard A Kahn
Mitochondria are essential, dynamic organelles that respond to a number of stressors with changes in morphology that are linked to several mitochondrial functions, though the mechanisms involved are poorly understood. We show that the levels of the regulatory GTPase ARL2 and its GAP, ELMOD2, are specifically increased at mitochondria in immortalized mouse embryo fibroblasts deleted for Mitofusin 2 (MFN2), but not MFN1. Elevated ARL2 and ELMOD2 in MEFs deleted for MFN2 could be reversed by re-introduction of MFN2, but only when the mitochondrial fragmentation in these MEFs was also reversed, demonstrating that reversal of elevated ARL2 and ELMOD2 requires the fusogenic activity of MFN2...
2017: PloS One
https://www.readbyqxmd.com/read/28379197/abnormalities-of-mitochondrial-dynamics-in-neurodegenerative-diseases
#14
REVIEW
Ju Gao, Luwen Wang, Jingyi Liu, Fei Xie, Bo Su, Xinglong Wang
Neurodegenerative diseases are incurable and devastating neurological disorders characterized by the progressive loss of the structure and function of neurons in the central nervous system or peripheral nervous system. Mitochondria, organelles found in most eukaryotic cells, are essential for neuronal survival and are involved in a number of neuronal functions. Mitochondrial dysfunction has long been demonstrated as a common prominent early pathological feature of a variety of common neurodegenerative diseases, including Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), and Huntington's disease (HD)...
April 5, 2017: Antioxidants (Basel, Switzerland)
https://www.readbyqxmd.com/read/28348166/mfn2-is-critical-for-brown-adipose-tissue-thermogenic-function
#15
Marie Boutant, Sameer S Kulkarni, Magali Joffraud, Joanna Ratajczak, Miriam Valera-Alberni, Roy Combe, Antonio Zorzano, Carles Cantó
Mitochondrial fusion and fission events, collectively known as mitochondrial dynamics, act as quality control mechanisms to ensure mitochondrial function and fine-tune cellular bioenergetics. Defective mitofusin 2 (Mfn2) expression and enhanced mitochondrial fission in skeletal muscle are hallmarks of insulin-resistant states. Interestingly, Mfn2 is highly expressed in brown adipose tissue (BAT), yet its role remains unexplored. Using adipose-specific Mfn2 knockout (Mfn2-adKO) mice, we demonstrate that Mfn2, but not Mfn1, deficiency in BAT leads to a profound BAT dysfunction, associated with impaired respiratory capacity and a blunted response to adrenergic stimuli...
March 27, 2017: EMBO Journal
https://www.readbyqxmd.com/read/28342806/molecular-regulation-of-mitochondrial-dynamics-in-cardiac-disease
#16
REVIEW
Jinliang Nan, Wei Zhu, M S Rahman, Mingfei Liu, Dan Li, Shengan Su, Na Zhang, Xinyang Hu, Hong Yu, Mahesh P Gupta, Jian'an Wang
Mitochondrial homeostasis is critical for keeping functional heart in response to metabolic or environmental stresses. Mitochondrial fission and fusion (mitochondrial dynamics) play essential roles in maintaining mitochondrial homeostasis, defects in mitochondrial dynamics lead to cardiac diseases such as ischemia-reperfusion injury (IRI), heart failure and diabetic cardiomyopathy. Mitochondrial dynamics is determined by mitochondrial fission and fusion proteins, including OPA1, mitofusins and Drp1. These proteins are tightly regulated by a series of signaling pathways through different aspects such as transcription, post translation modifications (PTMs) and proteasome-dependent protein degradation...
March 22, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28324764/enhancing-mitofusin-marf-ameliorates-neuromuscular-dysfunction-in-drosophila-models-of-tdp-43-proteinopathies
#17
Bilal Khalil, Marie-Jeanne Cabirol-Pol, Laetitia Miguel, Alexander J Whitworth, Magalie Lecourtois, Jean-Charles Liévens
Transactive response DNA-binding protein 43 kDa (TDP-43) is considered a major pathological protein in amyotrophic lateral sclerosis and frontotemporal lobar degeneration. The precise mechanisms by which TDP-43 dysregulation leads to toxicity in neurons are not fully understood. Using TDP-43-expressing Drosophila, we examined whether mitochondrial dysfunction is a central determinant in TDP-43 pathogenesis. Expression of human wild-type TDP-43 in Drosophila neurons results in abnormally small mitochondria...
June 2017: Neurobiology of Aging
https://www.readbyqxmd.com/read/28322724/valosin-containing-protein-vcp-p97-inhibitors-relieve-mitofusin-dependent-mitochondrial-defects-due-to-vcp-disease-mutants
#18
Ting Zhang, Prashant Mishra, Bruce A Hay, David Chan, Ming Guo
Missense mutations of valosin-containing protein (VCP) cause an autosomal dominant disease known as inclusion body myopathy, Paget disease with frontotemporal dementia (IBMPFD) and other neurodegenerative disorders. The pathological mechanism of IBMPFD is not clear and there is no treatment. We show that endogenous VCP negatively regulates Mitofusin, which is required for outer mitochondrial membrane fusion. Because 90% of IBMPFD patients have myopathy, we generated an in vivo IBMPFD model in adult Drosophila muscle, which recapitulates disease pathologies...
March 21, 2017: ELife
https://www.readbyqxmd.com/read/28292876/maternal-exercise-upregulates-mitochondrial-gene-expression-and-increases-enzyme-activity-of-fetal-mouse-hearts
#19
Eunhee Chung, Hayli E Joiner, Tracer Skelton, Kalli D Looten, Maria Manczak, P Hemachandra Reddy
Maternal exercise during pregnancy has been shown to improve the long-term health of offspring in later life. Mitochondria are important organelles for maintaining adequate heart function, and mitochondrial dysfunction is linked to cardiovascular disease. However, the effects of maternal exercise during pregnancy on mitochondrial biogenesis in hearts are not well understood. Thus, the purpose of this study was to test the hypothesis that mitochondrial gene expression in fetal myocardium would be upregulated by maternal exercise...
March 2017: Physiological Reports
https://www.readbyqxmd.com/read/28289205/reply-to-filadi-et-al-does-mitofusin-2-tether-or-separate-endoplasmic-reticulum-and-mitochondria
#20
Deborah Naon, Marta Zaninello, Marta Giacomello, Tatiana Varanita, Francesca Grespi, Sowmya Lakshminaranayan, Annalisa Serafini, Martina Semenzato, Stephanie Herkenne, Maria Isabel Hernández-Alvarez, Antonio Zorzano, Diego De Stefani, Gerald W Dorn, Luca Scorrano
No abstract text is available yet for this article.
March 21, 2017: Proceedings of the National Academy of Sciences of the United States of America
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