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Mitochondrial fission

Ling Chien, Min-Zong Liang, Chu-Yuan Chang, Chen Wang, Linyi Chen
Due to the inhibitory microenvironment and reduced intrinsic growth capacity of neurons, neuronal regeneration of central nervous system remains challenging. Neurons are highly energy demanding and require sufficient mitochondria to support cellular activities. In response to stimuli, mitochondria undergo fusion/fission cycles to adapt to environment. It is thus logical to hypothesize that the plasticity of mitochondrial dynamics is required for neuronal regeneration. In this study, we examined the role of mitochondrial dynamics during regeneration of rat hippocampal neurons...
June 15, 2018: Biochimica et Biophysica Acta
Dong Gil Lee, Min Kyoung Kam, Kyung Min Kim, Han Seop Kim, Oh-Shin Kwon, Hyun-Shik Lee, Dong-Seok Lee
Iron is an essential element for neuronal as well as cellular functions. However, Iron overload has been known to cause neuronal toxicity through mitochondrial fission, dysregulation of Ca2+ , endoplasmic reticulum (ER) stress, and reactive oxygen species (ROS) production. Nevertheless, the precise mechanisms of iron-induced oxidative stress and mitochondria- and ER-related iron toxicity in neuronal cells are not fully understood. In this study, we demonstrated that iron overload induces ROS production earlier in the ER than in the mitochondria, and peroxiredoxin 5 (Prx5), which is a kind of antioxidant induced by iron overload, prevents iron overload-induced mitochondrial fragmentation mediated by contact with ER and translocation of Drp1, by inhibiting ROS production and calcium/calcineurin pathway in HT-22 mouse hippocampal neuronal cells...
June 12, 2018: International Journal of Biochemistry & Cell Biology
Matthias Hecker, Natascha Sommer, Sebastian Foch, Andreas Hecker, Holger Hackstein, Martin Witzenrath, Norbert Weissmann, Werner Seeger, Konstantin Mayer
Inflammatory disorders such as sepsis are a major cause of morbidity and mortality. Mitochondrial dysfunction is considered a key factor in the pathogenesis of severe inflammation. In the present study, we aimed to investigate the impact of arachidonic acid, omega-3 (n-3) fatty acids, and n-3-derived lipid mediators 18R-HEPE and resolvin (Rv) E1 on mitochondrial function in experimental inflammation. The results revealed that, in contrast to n-6 and n-3 fatty acids, both 18R-HEPE and RvE1 possess anti-inflammatory and anti-apoptotic properties...
June 11, 2018: Biochimica et Biophysica Acta
Raghav Kalia, Ray Yu-Ruei Wang, Ali Yusuf, Paul V Thomas, David A Agard, Janet M Shaw, Adam Frost
Mitochondrial inheritance, genome maintenance and metabolic adaptation depend on organelle fission by dynamin-related protein 1 (DRP1) and its mitochondrial receptors. DRP1 receptors include the paralogues mitochondrial dynamics proteins of 49 and 51 kDa (MID49 and MID51) and mitochondrial fission factor (MFF); however, the mechanisms by which these proteins recruit and regulate DRP1 are unknown. Here we present a cryo-electron microscopy structure of full-length human DRP1 co-assembled with MID49 and an analysis of structure- and disease-based mutations...
June 13, 2018: Nature
Jae Ho Seo, Ekta Agarwal, Kelly G Bryant, M Cecilia Caino, Eui Tae Kim, Andrew V Kossenkov, Hsin-Yao Tang, Lucia R Languino, Dmitry I Gabrilovich, Andrew R Cohen, David W Speicher, Dario C Altieri
Syntaphilin (SNPH) inhibits the movement of mitochondria in tumor cells, preventing their accumulation at the cortical cytoskeleton and limiting the bioenergetics of cell motility and invasion. Although this may suppress metastasis, the regulation of the SNPH pathway is not well understood. Using a global proteomics screen, we show that SNPH associates with multiple regulators of ubiquitin-dependent responses and is ubiquitinated by the E3 ligase CHIP (or STUB1) on Lys111 and Lys153 in the microtubule-binding domain...
June 13, 2018: Cancer Research
Najla El Fissi, Manuel Rojo, Aїcha Aouane, Esra Karatas, Gabriela Poliacikova, Claudine David, Julien Royet, Thomas Rival
Charcot-Marie-Tooth disease type 2A (CMT2A) is caused by dominant alleles of the mitochondrial pro-fusion factor Mitofusin 2 (MFN2). To address the consequences of these mutations on mitofusin activity and neuronal function, we generate Drosophila models expressing in neurons the two most frequent substitutions (R94Q and R364W, the latter never studied before) and two others localizing to similar domains (T105M and L76P). All alleles trigger locomotor deficits associated with mitochondrial depletion at neuromuscular junctions, decreased oxidative metabolism and increased mtDNA mutations, but they differently alter mitochondrial morphology and organization...
June 13, 2018: EMBO Reports
Shiyuan Huang, Xiaona Wang, Xinmei Wu, Jiale Yu, JinJing Li, Xiaoyuan Huang, Chunfang Zhu, Hongshan Ge
Yes-associated protein (Yap) was the core transcriptional co-activator in the downstream Hippo pathway that regulated cell proliferation and tissue growth. However, its role in the regulation of myoblast differentiation remains unclear. Regulation of mitochondrial networks by dynamin-related protein 1 (Drp1) and mitofusion 2 (Mfn2) is crucial for the activation of myoblast differentiation. In the present study, we investigated the interplay between the Hippo-Yap pathway and protein contents of Mfn2 and Drp1 during myoblast differentiation...
June 13, 2018: American Journal of Physiology. Cell Physiology
Chinthasagar Bastian, Jane Zaleski, Katharine Stahon, Brandon Parr, Andrew McCray, Jerica Day, Sylvain Brunet, Selva Baltan
White matter (WM) damage following a stroke underlies a majority of the neurological disability that is subsequently observed. Although ischemic injury mechanisms are age-dependent, conserving axonal mitochondria provides consistent post-ischemic protection to young and aging WM. Nitric Oxide Synthase (NOS) activation is a major cause of oxidative and mitochondrial injury in gray matter during ischemia; therefore, we used a pure WM tract, isolated male mouse optic nerve, to investigate whether NOS inhibition provides post-ischemic functional recovery by preserving mitochondria...
June 11, 2018: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
Ze Liu, Hao Li, Jianqun Su, Shihui Xu, Fengxin Zhu, Jun Ai, Zheng Hu, Miaomiao Zhou, Jianwei Tian, Zhiyuan Su, Peiliang Yang, Jing Nie
AIMS: Mitochondrial fragmentation is a crucial mechanism contributing to tubular cell apoptosis during acute kidney injury (AKI). However, the mechanism of modulating mitochondrial dynamics during AKI remains unclear. Numb is a multifunction adaptor protein that is expressed in renal tubules. The aim of the present study is to study the role of Numb in mitochondrial dysfunction during AKI. RESULTS: The expression of Numb was upregulated in both ischemia-reperfusion- and cisplatin-induced AKI...
June 11, 2018: Antioxidants & Redox Signaling
Elisabet Cuyàs, Sara Verdura, Núria Folguera-Blasco, Cristian Bastidas-Velez, Ángel G Martin, Tomás Alarcón, Javier A Menendez
Unraveling the key mechanisms governing the retention versus loss of the cancer stem cell (CSC) state would open new therapeutic avenues to eradicate cancer. Mitochondria are increasingly recognized key drivers in the origin and development of CSC functional traits. We here propose the new term "mitostemness" to designate the mitochondria-dependent signaling functions that, evolutionary rooted in the bacterial origin of mitochondria, regulate the maintenance of CSC self-renewal and resistance to differentiation...
June 9, 2018: Cell Cycle
Hye Yun Jeong, Jun Mo Kang, Hak Hoon Jun, Dong-Jin Kim, Seon Hwa Park, Min Ji Sung, Jin Hyung Heo, Dong Ho Yang, Sang Ho Lee, So-Young Lee
We investigated the effects of chloroquine (CQ) and amodiaquine (AQ) on AMPK phosphorylation in renal tubular cells in a diabetic environment in vivo and in vitro. We also examined whether CQ- or AQ-mediated AMPK activity restoration attenuated diabetic tubulopathy by normalizing mitochondrial fragmentation. Human renal proximal epithelial cells (HKC8) were incubated in high-glucose conditions. Diabetes was induced with streptozotocin in male C57/BL6J mice. Treatment with CQ or AQ abolished high-glucose-induced phospho-AMPK and phosph-PGC1α down-regulation in HKC8 cells...
June 8, 2018: Scientific Reports
Tian Feng, Toru Yamashita, Yun Zhai, Jingwei Shang, Yumiko Nakano, Ryuta Morihara, Yusuke Fukui, Nozomi Hishikawa, Yasuyuki Ohta, Koji Abe
Mitochondrial dynamically undergo massive fusion and fission events to continuously maintain their function in cells. Although an impaired balance of mitochondrial fission and fusion was reported in in-vitro and in-vivo Alzheimer's disease (AD) model, changes of mitochondrial fission and fusion proteins have not been reported in AD with chronic cerebral hypoperfusion (HP) as an etiological factor related to the development of elder AD. To clarify the impacts of HP on mitochondrial fission and fusion, related oxidative stress in the pathogenesis of AD, and protective effect of galantamine, the novel AD with HP mouse model (APP23 + HP) was applied in this project...
June 4, 2018: Brain Research
Yang Su, Jie Chen, Ying Huang
Pentatricopeptide repeat (PPR) proteins are major players in mitochondrial and chloroplast RNA metabolism which is essential for normal organellar function. The fission yeast Schizosaccharomyces pombe has ten PPR proteins. We have previously reported that loss of ppr3, ppr4, ppr6, or ppr10 perturbs iron homeostasis leading to accumulation of reactive oxygen species and apoptotic cell death. In the present study, we show that loss of ppr3, ppr4, ppr6, or ppr10 can cause non-sexual flocculation and filamentous growth of cells...
June 6, 2018: FEMS Microbiology Letters
Conor S Ryan, Anthony L Fine, Alexander L Cohen, Brenda M Schiltz, Deborah L Renaud, Elaine C Wirrell, Marc C Patterson, Nicole J Boczek, Raymond Liu, Dusica Babovic-Vuksanovic, David C Chan, Eric T Payne
BACKGROUND: The dynamin 1-like gene ( DNM1L) encodes a GTPase that mediates mitochondrial and peroxisomal fission and fusion. We report a new clinical presentation associated with a DNM1L pathogenic variant and review the literature. RESULTS: A 13-year-old boy with mild developmental delays and paroxysmal dystonia presented acutely with multifocal myoclonic super-refractory status epilepticus. Despite sustained and aggressive treatment, seizures persisted and care was ultimately withdrawn in the context of extensive global cortical atrophy...
January 1, 2018: Journal of Child Neurology
Jingwei Song, Xiaowen Lei, Wei Jiao, Yafang Song, Weijing Chen, Jinqiu Li, Zhiwei Chen
Myasthenia gravis (MG) is an autoimmune neuromuscular disease characterized by the production of antibodies against acetylcholine receptors (AChRs). Qiangji Jianli (QJJL) decoction is an effective traditional Chinese medicine (TCM) that is used to treat MG. Our study aimed to investigate the effect of QJJL decoction on MG and to clarify the mechanism by which QJJL regulates mitochondrial energy metabolism and mitochondrial fusion and fission (MFF). SPF female Lewis rats were administered Rat 97-116 peptides to induce experimental autoimmune myasthenia gravis (EAMG)...
June 5, 2018: Scientific Reports
Yi-Tong Lu, Lan-Zhu Li, Yi-Lin Yang, Xiaojian Yin, Qun Liu, Lei Zhang, Kang Liu, Baolin Liu, Jia Li, Lian-Wen Qi
Altered mitochondrial metabolism acts as an initial cause for cardiovascular diseases and metabolic intermediate succinate emerges as a mediator of mitochondrial dysfunction. This work aims to investigate whether or not extracellular succinate accumulation and its targeted G protein-coupled receptor-91 (GPR91) activation induce cardiac injury through mitochondrial impairment. The results showed that extracellular succinate promoted the translocation of dynamin-related protein 1 (Drp1) to mitochondria via protein kinase Cδ (PKCδ) activation, and induced mitochondrial fission factor (MFF) phosphorylation via extracellular signal-regulated kinases-1/2 (ERK1/2) activation in a GPR91-dependent manner...
June 4, 2018: Cell Death & Disease
Hao Zhao, Yongchun Luo, Lihua Chen, Zhenhai Zhang, Chunsen Shen, Yunjun Li, Ruxiang Xu
Cerebral ischemia-reperfusion injury (IRI) potentiates existing brain damage and increases mortality and morbidity via poorly understood mechanisms. The aim of our study is to investigate the role of Sirtuin 3 (Sirt3) in the development and progression of cerebral ischemia-reperfusion injury with a focus on mitochondrial fission and the Wnt/β-catenin pathway. Our data indicated that Sirt3 was downregulated in response to cerebral IRI. However, the overexpression of Sirt3 reduced the brain infarction area and repressed IRI-mediated neuron apoptosis...
June 3, 2018: Cell Stress & Chaperones
Feng Min, Wang Lirui, Chang Siyuan, Yuan Pu
AIM: The potential mechanism of penehyclidine hydrochloride (PHC) against myocardial ischemia-reperfusion (I/R) injury has not been fully elucidated. The aim of the present study was to reveal whether mitochondrial dynamics, apoptosis, and MAPKs were involved in the cardioprotective effect of this drug on myocardial I/R injury. METHODS: Ninety healthy adult male Wistar rats were separately pretreated with normal saline (0.9%); PHC; and signal pathway blockers of MAPKs, Drp1, and Bcl-2...
May 31, 2018: European Journal of Pharmaceutical Sciences
Tadato Ban, Hiroto Kohno, Takaya Ishihara, Naotada Ishihara
Mitochondria are highly dynamic organelles that undergo frequent fusion and fission. The large GTPase optic atrophy 1 (OPA1) is identified as a core component of inner membrane (IM) fusion. OPA1 exists as the membrane-anchored L-OPA1 and the proteolytically cleavage soluble S-OPA1. Recently, we showed that OPA1 and mitochondria-localized lipid cardiolipin (CL) cooperate in heterotypic IM fusion [Ban et al., Nat. Cell Biol. 19 (2017) 856-863]. We reconstituted an in vitro membrane fusion reaction using purified human L-OPA1 and S-OPA1 expressed in silkworm and found that L-OPA1 on one side of the membrane and CL on the other side were sufficient for mitochondrial fusion...
May 28, 2018: Biochimica et Biophysica Acta
Luca Simula, Silvia Campello
Mitochondria exist in a dynamic state inside mammalian cells. They undergo processes of fusion and fission to adjust their shape according to the different cell needs. Different proteins tightly regulate these dynamics: Opa-1 and Mitofusin-1 and Mitofusin-2 are the main profusion proteins, while Drp1 and its different receptors (Mff, Fis1, MiD49, MiD51) regulate mitochondrial fission. The dynamic nature of the mitochondrial network has become evident and detectable, thanks to recent advances in live imaging video microscopy and to the availability of mitochondria-tagged fluorescent proteins...
2018: Methods in Molecular Biology
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