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Mitochondria fission

Adeline Jacquet, Cécile Cottet-Rousselle, Josiane Arnaud, Kevin Julien Saint Amand, Raoua Ben Messaoud, Marine Lénon, Christine Demeilliers, Jean-Marc Moulis
The impact of chronic cadmium exposure and slow accumulation on the occurrence and development of diabetes is controversial for human populations. Islets of Langerhans play a prominent role in the etiology of the disease, including by their ability to secrete insulin. Conversion of glucose increase into insulin secretion involves mitochondria. A rat model of pancreatic β-cells was exposed to largely sub-lethal levels of cadmium cations applied for the longest possible time. Cadmium entered cells at concentrations far below those inducing cell death and accumulated by factors reaching several hundred folds the basal level...
March 22, 2018: Toxics
Perry G Ridge, John S K Kauwe
Purpose of Review: Alzheimer's disease (AD) is the most common form of dementia, affects an increasing number of people worldwide, has a rapidly increasing incidence, and is fatal. In the past several years, significant progress has been made towards solving the genetic architecture of AD, but our understanding remains incomplete and has not led to treatments that either cure or slow disease. There is substantial evidence that mitochondria are involved in AD: mitochondrial functional declines in AD, mitochondrial encoded gene expression changes, mitochondria are morphologically different, and mitochondrial fusion/fission are modified...
2018: Current Genetic Medicine Reports
Yinfang Wang, Yitong Huang, Youbin Liu, Jinping Li, Yilong Hao, Peihao Yin, Zongjun Liu, Jingzhou Chen, Ying Wang, Nanping Wang, Peng Zhang
Mitochondria are dynamic organelles that are able to change their morphology and cellular distribution by either fission or fusion. However, the molecular mechanisms controlling mitochondrial dynamics in vascular endothelial cells (ECs) remain largely unknown. In this study, we observed that knock down of microtubule-associated tumor suppressor 1 (MTUS1) in ECs inhibited tube formation and migration, accompanied with decreased promigratory signalings. We showed that MTUS1 was localized in the outer membrane of mitochondria in ECs...
March 20, 2018: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
Saki Hirofuji, Yuta Hirofuji, Hiroki Kato, Keiji Masuda, Haruyoshi Yamaza, Hiroshi Sato, Fumiko Takayama, Michiko Torio, Yasunari Sakai, Shouichi Ohga, Tomoaki Taguchi, Kazuaki Nonaka
Rett syndrome is an X-linked neurodevelopmental disorder associated with psychomotor impairments, autonomic dysfunctions and autism. Patients with Rett syndrome have loss-of-function mutations in MECP2, the gene encoding methyl-CpG-binding protein 2 (MeCP2). Abnormal biogenic amine signaling and mitochondrial function have been found in patients with Rett syndrome; however, few studies have analyzed the association between these factors. This study investigated the functional relationships between mitochondria and the neuronal differentiation of the MeCP2-deficient stem cells from the exfoliated deciduous teeth of a child with Rett syndrome...
March 10, 2018: Biochemical and Biophysical Research Communications
Seokjo Kang, Jayoung Byun, Sung Min Son, Inhee Mook-Jung
Alzheimer's disease (AD) is often characterized by the impairment of mitochondrial function caused by excessive mitochondrial fragmentation. Thrombospondin-1 (TSP-1), which is primarily secreted from astrocytes in the central nervous system (CNS), has been suggested to play a role in synaptogenesis, spine morphology, and synaptic density of neurons. In this study, we investigate the protective role of TSP-1 in the recovery of mitochondrial morphology and function in amyloid β (Aβ)-treated mouse hippocampal neuroblastoma cells (HT22)...
December 2018: Cell Death Discovery
Antonietta Franco, Daniela Sorriento, Jessica Gambardella, Roberto Pacelli, Nella Prevete, Claudio Procaccini, Giuseppe Matarese, Bruno Trimarco, Guido Iaccarino, Michele Ciccarelli
The modern understanding of the G protein-coupled receptor kinase 2 has grown towards the definition of a stress protein, for its ability to rapidly compartmentalize within the cell in response to acute stimulation. Also, mitochondria can be regulated by GRK2 localization. We show that Ionizing Radiation (IR) exposure acutely damages mitochondria regarding mass, morphology, and respiration, with recovery in a framework of hours. This phenomenon is actively regulated by GRK2, whose overexpression results to be protective, and reciprocally, deletion accelerates degenerative processes...
December 2018: Cell Death Discovery
Summer J Rozzi, Valeria Avdoshina, Jerel A Fields, Italo Mocchetti
Human immunodeficiency virus-1 (HIV) infection of the central nervous system promotes neuronal injury that culminates in HIV-associated neurocognitive disorders. Viral proteins, including transactivator of transcription (Tat), have emerged as leading candidates to explain HIV-mediated neurotoxicity, though the mechanisms remain unclear. Tat transgenic mice or neurons exposed to Tat, which show neuronal loss, exhibit smaller mitochondria as compared to controls. To provide an experimental clue as to which mechanisms are used by Tat to promote changes in mitochondrial morphology, rat cortical neurons were exposed to Tat (100 nM) for various time points...
December 2018: Cell Death Discovery
YuZhen Li, XiuHua Liu
As the main source of energy in the body, mitochondria are highly dynamic organelles, which are constantly going through fusion and fission. The fine balance of mitochondrial fusion and fission plays an important role in maintaining the stability of cardiomyocyte homeostasis. The processes of mitochondrial fusion and fission are very complex, which is mediated by fusion and fission proteins. Disruptions in these processes through controlling fusion and fission proteins affect mitochondrial functions and cardiomyocyte survival...
March 12, 2018: Journal of Cellular Physiology
Benjamin Gottschalk, Christinae Klec, Markus Waldeck-Weiermair, Roland Malli, Wolfgang F Graier
Mitochondria are multifunctional organelles that essentially contribute to cell signaling by sophisticated mechanisms of communications. Live cell imaging studies showed that mitochondria are dynamic and complex structures that form ramified networks by directed movements, fission, and fusion events. There is emerging evidence that the morphology of mitochondria determines cellular functions and vice versa. Several intracellular signaling pathways and messengers including Ca2+ dynamically influence the architecture of mitochondria...
March 12, 2018: Pflügers Archiv: European Journal of Physiology
Jeong-Min Hong, Sun-Mee Lee
AIMS: Heme oxygenase-1 (HO-1), an endogenous cytoprotective enzyme, is reported that can be localized in mitochondria under stress, contributing to preserve mitochondrial function. Mitochondrial quality control (QC) is essential to cellular health and recovery linked with redox homeostasis. Recent studies reported that phosphoglycerate mutase family member (PGAM) 5, a mitochondria-resident phosphatase, plays critical role in mitochondrial homeostasis. Therefore, we aim to investigate cytoprotective mechanisms of HO-1 in I/R-induced hepatic injury focusing on mitochondrial QC associated with PGAM5 signaling...
March 7, 2018: Life Sciences
Francesca Martorana, Daniela Gaglio, Maria Rosaria Bianco, Federica Aprea, Assunta Virtuoso, Marcella Bonanomi, Lilia Alberghina, Michele Papa, Anna Maria Colangelo
Neuronal differentiation involves extensive modification of biochemical and morphological properties to meet novel functional requirements. Reorganization of the mitochondrial network to match the higher energy demand plays a pivotal role in this process. Mechanisms of neuronal differentiation in response to nerve growth factor (NGF) have been largely characterized in terms of signaling, however, little is known about its impact on mitochondrial remodeling and metabolic function. In this work, we show that NGF-induced differentiation requires the activation of autophagy mediated by Atg9b and Ambra1, as it is disrupted by their genetic knockdown and by autophagy blockers...
March 9, 2018: Cell Death & Disease
Jie Gao, Ailin Luo, Jing Yan, Xi Fang, Xiaole Tang, Yilin Zhao, Shiyong Li
Accumulating evidence indicates that general anesthetics can cause acute neuroapoptosis and long-term cognitive deficit in models exposed to anesthetics during the brain growth-spurt period. Anesthetics-induced imbalance of mitochondrial fusion and fission preceded and contributed to developmental neuroapoptosis. Accordingly, the imbalance was accompanied by activation of dynamin-related protein (Drp)1 which was closely associated with synaptic degeneration in neurodegenerative diseases. Based on the neuroprotective role of mitochondrial division inhibitor-1 (mdivi-1) in neurodegeneration and stroke, we set out to examine whether mdivi-1 can mitigate developmental neurotoxicity induced by isoflurane...
2018: American Journal of Translational Research
Aurel Popa-Wagner, Raluca E Sandu, Coman Cristin, Adriana Uzoni, Kevin A Welle, Jennifer R Hryhorenko, Sina Ghaemmaghami
Brain structures differ in the magnitude of age-related neuron loss with the cerebellum being more affected. An underlying cause could be an age-related decline in mitochondrial bioenergetics. Successful aging of mitochondria reflects a balanced turnover of proteins involved in mitochondrial biogenesis and mitophagy. Thus, an imbalance in mitochondrial turnover can contribute to the diminution of cellular function seen during aging. Mitochondrial biogenesis and mitophagy are mediated by a set of proteins including MFN1, MFN2, OPA1, DRP1, FIS1 as well as DMN1l and DNM1, all of which are required for mitochondrial fission...
2018: Frontiers in Aging Neuroscience
Yulai Shen, Lu Wu, Jun Wang, Xin Wu, Xuemei Zhang
Methamphetamine (METH) abuse causes significant physical, psychological, and social concerns. Therefore, in this study, we investigated its effects on osteogenic differentiation of mesenchymal stem cells (MSCs). We found that METH dose-dependently affected MSCs viability. Upon osteogenic induction, the 3 and 30 µmol/l METH dosages without deleterious effects on MSCs viability resulted in the down-regulation of osteoblastic marker genes (Alp, Bglap, and Runx2), suppression of the protein expression of RUNX2, and decreased ALP activity and mineralization ability...
March 1, 2018: European Journal of Pharmacology
Yan G Zhao, Hong Zhang
The ER forms contacts with other endomembrane systems to exchange materials (e.g., calcium and lipids) and also to modulate dynamic organelle processes, including fission, cargo sorting and movement. During autophagosome formation, dynamic contacts between the ER and the phagophore membrane are crucial for phagophore expansion and closure. Little is known about the mechanisms underlying the formation and disassembly of the ER contacts. We found that the ER-localized autophagy protein EPG-3/VMP1 plays an essential role in controlling ER-phagophore dissociation and also the disassembly of ER contacts with LDs, mitochondria and endolysosomes...
March 1, 2018: Autophagy
Denis Martinvalet
Mitochondria and endoplasmic reticulum (ER) contact sites (MERCs) are dynamic modules enriched in subset of lipids and specialized proteins that determine their structure and functions. The MERCs regulate lipid transfer, autophagosome formation, mitochondrial fission, Ca2+ homeostasis and apoptosis. Since these functions are essential for cell biology, it is therefore not surprising that MERCs also play a critical role in organ physiology among which the immune system stands by its critical host defense function...
February 28, 2018: Cell Death & Disease
Riccardo Filadi, Diana Pendin, Paola Pizzo
Mitochondria are highly dynamic organelles whose functions are essential for cell viability. Within the cell, the mitochondrial network is continuously remodeled through the balance between fusion and fission events. Moreover, it dynamically contacts other organelles, particularly the endoplasmic reticulum, with which it enterprises an important functional relationship able to modulate several cellular pathways. Being mitochondria key bioenergetics organelles, they have to be transported to all the specific high-energy demanding sites within the cell and, when damaged, they have to be efficiently removed...
February 28, 2018: Cell Death & Disease
Diego Grassi, Shannon Howard, Minghai Zhou, Natalia Diaz-Perez, Nicolai T Urban, Debbie Guerrero-Given, Naomi Kamasawa, Laura A Volpicelli-Daley, Philip LoGrasso, Corinne Ida Lasmézas
Exposure of cultured primary neurons to preformed α-synuclein fibrils (PFFs) leads to the recruitment of endogenous α-synuclein and its templated conversion into fibrillar phosphorylated α-synuclein (pα-synF) aggregates resembling those involved in Parkinson's disease (PD) pathogenesis. Pα-synF was described previously as inclusions morphologically similar to Lewy bodies and Lewy neurites in PD patients. We discovered the existence of a conformationally distinct, nonfibrillar, phosphorylated α-syn species that we named "pα-syn*...
February 27, 2018: Proceedings of the National Academy of Sciences of the United States of America
Pedro Scarpelli, Giulliana Tessarin Almeida, Kênia Lopes Viçoso, Wania Rezende Lima, Lucas Borges Pereira, Kamila Anna Meissner, Carsten Wrenger, Anna Rafaello, Rosario Rizzuto, Tullio Pozzan, Celia R S Garcia
Malaria causes millions of deaths worldwide and is considered a huge burden to underdeveloped countries. The number of cases with resistance to all antimalarials is continuously increasing, making the identification of novel drugs a very urgent necessity. A potentially very interesting target for novel therapeutic intervention is the parasite mitochondrion. In this work we studied in P. falciparum three genes coding for proteins homologues of the mammalian FIS1 (Mitochondrial Fission Protein 1) and DRP1 (Dynamin Related Protein 1) involved in mitochondrial fission...
February 26, 2018: Journal of Pineal Research
Jean-Philippe Leduc-Gaudet, Olivier Reynaud, François Chabot, Jocelyne Mercier, David E Andrich, David H St-Pierre, Gilles Gouspillou
Multiple aspects of mitochondrial function and dynamics remain poorly studied in the skeletal muscle of pediatric models in response to a short-term high-fat diet (HFD). This study investigated the impact of a short-term HFD on mitochondrial function and dynamics in the oxidative soleus (SOL) and glycolytic extensor digitorum longus (EDL) muscles in young rats. Young male Wistar rats were submitted to either HFD or normal chow (NCD) diets for 14 days. Permeabilized myofibers from SOL and EDL were prepared to assess mitochondrial respiration and reactive oxygen species (ROS) production...
February 2018: Physiological Reports
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