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Aging mitochondria

Jacques Joyard, Hartmut K Lichtenthaler
On November 4, 2018, Roland Douce, Professor Emeritus at the University of Grenoble, France, died at the age of 79. In Grenoble, where he spent most of his scientific career, Roland Douce created a world-renowned school of plant science, studying the structure, functions, and interactions of plant organelles involved in photosynthesis, respiration, and photorespiration. His main achievements concern the chemical and functional characterization of chloroplast envelope membranes, the demonstration of the uniqueness of plant mitochondria, and the integration of metabolism within the plant cell, among manifold activities...
March 15, 2019: Photosynthesis Research
Emmanuelle C Genin, Blandine Madji Hounoum, Sylvie Bannwarth, Konstantina Fragaki, Sandra Lacas-Gervais, Alessandra Mauri-Crouzet, Françoise Lespinasse, Julien Neveu, Baptiste Ropert, Gaelle Augé, Charlotte Cochaud, Cynthia Lefebvre-Omar, Stéphanie Bigou, Aude Chiot, Fanny Mochel, Séverine Boillée, Christian S Lobsiger, Delphine Bohl, Jean-Ehrland Ricci, Véronique Paquis-Flucklinger
Recently, we provided genetic basis showing that mitochondrial dysfunction can trigger motor neuron degeneration, through identification of CHCHD10 encoding a mitochondrial protein. We reported patients, carrying the p.Ser59Leu heterozygous mutation in CHCHD10, from a large family with a mitochondrial myopathy associated with motor neuron disease (MND). Rapidly, our group and others reported CHCHD10 mutations in amyotrophic lateral sclerosis (ALS), frontotemporal dementia-ALS and other neurodegenerative diseases...
March 14, 2019: Acta Neuropathologica
Ting Cao, Shuai Fan, Dong Zheng, Grace Wang, Yong Yu, Ruizhen Chen, Long-Sheng Song, Guo-Chang Fan, Zhuxu Zhang, Tianqing Peng
We and others have reported that calpain-1 was increased in myocardial mitochondria from various animal models of heart disease. This study investigated whether constitutive up-regulation of calpain-1 restricted to mitochondria induced myocardial injury and heart failure and, if so, whether these phenotypes could be rescued by selective inhibition of mitochondrial superoxide production. Transgenic mice with human CAPN1 up-regulation restricted to mitochondria in cardiomyocytes (Tg-mtCapn1/tTA) were generated and characterized with low and high over-expression of transgenic human CAPN1 restricted to mitochondria, respectively...
March 15, 2019: Basic Research in Cardiology
Jonas Mengel-From, Anne Marie Svane, Cino Pertoldi, Torsten Nygård Kristensen, Volker Loeschcke, Axel Skytthe, Kaare Christensen, Rune Lindahl-Jacobsen, Jacob Hjelmborg, Lene Christiansen
Aging is a multifactorial trait caused by early as well as late life circumstances. A society trend that parents deliberately delay having children is of concern to health professionals, e.g. since advanced parental age at conception increases disease risk profiles in offspring. We here aim to study if advanced parental age at conception affects mitochondria DNA content, a cross species biomarker of general health, in adult human twin offspring and in a model organism. We find no deteriorated mitochondria DNA content at advanced parental age at conception, but human mitochondria DNA content was higher in females than males, and the difference was two fold higher at advanced maternal age at conception...
March 15, 2019: Journals of Gerontology. Series A, Biological Sciences and Medical Sciences
Ramy K A Sayed, Marisol Fernández-Ortiz, María E Diaz-Casado, Paula Aranda-Martínez, José Fernández-Martínez, Ana Guerra-Librero, Germaine Escames, Luis C López, Reem M Alsaadawy, Darío Acuña-Castroviejo
To investigate the role of NLRP3 inflammasome in muscular aging, we evaluated here the morphological and functional markers of sarcopenia in the NLRP3-knockout mice, as well as the beneficial effect of melatonin supplementation. The gastrocnemius muscles of young (3 months), early-aged (12 months), and old-aged (24 months) NLRP3-knockout female mice were examined. Moreover, locomotor activity and apoptosis were assessed. The results revealed early markers of sarcopenia at the age of 12 months including reduction of lactate, ratio of muscle weight to body weight, muscle fibers number, and mitochondrial number...
March 14, 2019: Journals of Gerontology. Series A, Biological Sciences and Medical Sciences
Brooke E Hjelm, Brandi Rollins, Ling Morgan, Adolfo Sequeira, Firoza Mamdani, Filipe Pereira, Joana Damas, Michelle G Webb, Matthieu D Weber, Alan F Schatzberg, Jack D Barchas, Francis S Lee, Huda Akil, Stanley J Watson, Richard M Myers, Elizabeth C Chao, Virginia Kimonis, Peter M Thompson, William E Bunney, Marquis P Vawter
Deletions in the 16.6 kb mitochondrial genome have been implicated in numerous disorders that often display muscular and/or neurological symptoms due to the high-energy demands of these tissues. We describe a catalogue of 4489 putative mitochondrial DNA (mtDNA) deletions, including their frequency and relative read rate, using a combinatorial approach of mitochondria-targeted PCR, next-generation sequencing, bioinformatics, post-hoc filtering, annotation, and validation steps. Our bioinformatics pipeline uses MapSplice, an RNA-seq splice junction detection algorithm, to detect and quantify mtDNA deletion breakpoints rather than mRNA splices...
March 14, 2019: Nucleic Acids Research
Melvin R Hayden, DeAna G Grant, Annayya R Aroor, Vincent G DeMarco
Type 2 diabetes is associated with diabetic cognopathy. Anti-hyperglycemic sodium glucose transporter 2 (SGLT2) inhibitors have shown promise in reducing cognitive impairment in mice with type 2 diabetes mellitus. We recently described marked ultrastructural (US) remodeling of the neurovascular unit (NVU) in type 2 diabetic db / db female mice. Herein, we tested whether the SGLT-2 inhibitor, empagliflozin (EMPA), protects the NVU from abnormal remodeling in cortical gray and subcortical white matter. Ten-week-old female wild-type and db / db mice were divided into lean controls (CKC, n = 3), untreated db / db (DBC, n = 3), and EMPA-treated db / db (DBE, n = 3)...
March 7, 2019: Brain Sciences
Ewelina Prozorowska, Marlena Ratajczak, Hanna Jackowiak
The study describes the sequence of ultrastructural changes of the endometrial lining epithelium, first in the primordial paramesonephric ducts, then in the differentiating uterine horns, and finally in the mature uterus. The research material comprised female fetuses of the domestic cat, aged 33-63 days post conceptionem (p.c.), and mature females. The ultrastructural observations of the developing epithelium were conducted using transmission electron microscopy (TEM) and light microscopy (LM). The results revealed two basic stages in the development of the uterine mucosal epithelium in the domestic cat: the development of the epithelium of the uterine segment of the paramesonephric ducts, lasting from day 33 to day 42 p...
March 3, 2019: Theriogenology
M Bugliani, S Mossuto, F Grano, M Suleiman, L Marselli, U Boggi, P De Simone, D L Eizirik, M Cnop, P Marchetti, V De Tata
Autophagy is the major mechanism involved in degradation and recycling of intracellular components, and its alterations have been proposed to cause beta cell dysfunction. In this study, we explored the effects of autophagy modulation in human islets under conditions associated to endoplasmic reticulum (ER) stress. Human pancreatic islets were isolated by enzymatic digestion and density gradient purification from pancreatic samples of non-diabetic (ND; n = 17; age 65 ± 21 years; gender: 5 M/12 F; BMI 23.4 ± 3...
2019: Frontiers in Endocrinology
Carlos Vaamonde-García, María J López-Armada
Rheumatic and musculoskeletal diseases are a heterogeneous group of disorders affecting joint tissues and in some cases even organs, some of them being among the most common diseases worldwide. Mitochondria are the organelles considered as powerhouse of cells providing energy to the organism mainly through oxidative phosphorylation. However, mitochondria are also involved in crucial pathways responsible for maintaining cell physiology, such as the activation of metabolic and survival signaling, and innate and adaptive immune response...
March 9, 2019: Biochemical Pharmacology
Mayumi Takahashi, Kazuhide Takahashi
Mitochondrial function has been closely associated with normal aging and age-related diseases. Age-associated declines in mitochondrial function, such as changes in oxygen consumption rate, cytochrome c oxidase activity of complex IV, and mitochondrial coenzyme Q (CoQ) levels, begin as early as 12 to 15 months of age in male mouse brains. Brain mitochondrial dysfunction is accompanied by increased accumulation of phosphorylated α-synuclein in the motor cortex and impairment of motor activities, which are similar characteristics of Parkinson's disease...
March 11, 2019: Antioxidants (Basel, Switzerland)
Avery C Rossidis, Alessia Angelin, Kendall M Lawrence, Heron D Baumgarten, Aimee G Kim, Ali Y Mejaddam, Barbara E Coons, Heather A Hartman, Grace Hwang, Stylianos Monos, William H Peranteau, Marcus G Davey, Deborah Murdock, Douglas C Wallace, Alan W Flake
BACKGROUND: In an effort to mitigate the major morbidities and mortality associated with extreme prematurity, we have developed an EXTrauterine Environment for Neonatal Development (EXTEND) designed to provide physiologic support of extremely premature infants. OBJECTIVES: We have previously shown that long-term, physiologic support of premature fetal lambs is possible with EXTEND, but in this study, we sought to demonstrate bioenergetic equipoise at the tissue level...
March 12, 2019: Fetal Diagnosis and Therapy
Talisa Silzer, Robert Barber, Jie Sun, Gita Pathak, Leigh Johnson, Sid O'Bryant, Nicole Phillips
Mitochondrial function has been implicated and studied in numerous complex age-related diseases. Understanding the potential role of mitochondria in disease pathophysiology is of importance due to the rise in prevalence of complex age-related diseases, such as type 2 diabetes (T2D) and Alzheimer's disease (AD). These two diseases specifically share common pathophysiological characteristics which potentially point to a common root cause or factors for disease exacerbation. Studying the shared phenomena in Mexican Americans is of particular importance due to the disproportionate prevalence of both T2D and AD in this population...
2019: PloS One
Sebastian Wiberg, Nis Stride, John Bro-Jeppesen, Mathias J Holmberg, Jesper Kjærgaard, Steen Larsen, Michael W Donnino, Christian Hassager, Flemming Dela
BACKGROUND: While preclinical studies suggest that mitochondria play a pivotal role in ischaemia-reperfusion injury, the knowledge of mitochondrial function in human out-of-hospital cardiac arrest remains scarce. The present study sought to compare oxidative phosphorylation capacity in skeletal muscle biopsies from out-of-hospital cardiac arrest patients to healthy controls. METHODS: This was a substudy of a randomised trial comparing targeted temperature management at 33°C versus 36°C for out-of-hospital cardiac arrest patients...
March 11, 2019: European Heart Journal. Acute Cardiovascular Care
Mohammad Mohajeri, Cynthia Martín-Jiménez, George E Barreto, Amirhossein Sahebkar
Several lines of evidence have suggested that mitochondrial dysfunction plays a key role in neurodegeneration. The mitochondrial function is a potential target for steroid hormones, which could exert protective activities in the brain and other tissues. The decrease of some sex steroids with aging has been associated with deleterious effects on brain function and progression to neurodegenerative diseases. Recent in vitro and in vivo evidence provides the basis for this review on the interplay of sex steroids and mitochondrial defects in preventing or improving pathological events in the central nervous system (CNS)...
March 7, 2019: Progress in Neurobiology
Julia Kim, Emre Seli
Mitochondria play an essential role in generating energy for embryo development and maintaining embryo metabolism through key cellular functions including ion homeostasis, amino acid metabolism, glycolysis, fatty acid metabolism, signal transduction, and apoptotic regulation. Recent literature suggests that mitochondrial content and function may be related to implantation success and embryo viability. Some studies have linked increased levels of mitochondrial DNA to aneuploidy, advanced maternal age, and euploid blastocyst with implantation failure, while others have failed to demonstrate similar findings...
March 1, 2019: Reproduction: the Official Journal of the Society for the Study of Fertility
Nirmala Koju, Abdoh Taleb, Jifang Zhou, Ge Lv, Jie Yang, Xian Cao, Hui Lei, Qilong Ding
Reactive oxygen species (ROS) are the metabolites of oxygen that plays a significant role in cell signaling and homeostasis. Under normal conditions, ROS formation is stabilized by various antioxidant defense systems (ROS scavengers). Several studies in both in-vitro and in-vivo models, together with clinical data indicated that increased production ROS and oxidative stress plays a crucial role in the development and progression of endothelial dysfunction. The interactions between the main cellular sources of ROS, such as mitochondria and NADPH oxidases, however, remain unclear...
March 2019: Biomedicine & Pharmacotherapy
Anthea Di Rita, Flavie Strappazzon
During aging, the process of mitophagy, a system that allows the removal of dysfunctional mitochondria through lysosomal degradation, starts to malfunction. Because of this defect, damaged mitochondria are not removed correctly, and their decomposing components accumulate inside the cells. Dysfunctional mitochondria that are not removed by mitophagy produce high amounts of reactive oxygen species (ROS) and, thus, cause oxidative stress. Oxidative stress, in turn, is very harmful for the cells, neuronal cells, in particular...
March 6, 2019: Reviews in the Neurosciences
Joseph J Byrne, Ming S Soh, Gursimran Chandhok, Tarika Vijayaraghavan, Jean-Sébastien Teoh, Simon Crawford, Ansa E Cobham, Nethmi M B Yapa, Christen K Mirth, Brent Neumann
Mitochondria are essential components of eukaryotic cells, carrying out critical physiological processes that include energy production and calcium buffering. Consequently, mitochondrial dysfunction is associated with a range of human diseases. Fundamental to their function is the ability to transition through fission and fusion states, which is regulated by several GTPases. Here, we have developed new methods for the non-subjective quantification of mitochondrial morphology in muscle and neuronal cells of Caenorhabditis elegans...
March 6, 2019: Cellular and Molecular Life Sciences: CMLS
Chengjie Song, Jun Zhang, Shasha Qi, Zhen Liu, Xiaoyang Zhang, Yue Zheng, John-Paul Andersen, Weiping Zhang, Randy Strong, Paul Anthony Martinez, Nicolas Musi, Jia Nie, Yuguang Shi
Cardiolipin (CL) is a mitochondrial signature phospholipid that is required for membrane structure, respiration, dynamics, and mitophagy. Oxidative damage of CL by reactive oxygen species is implicated in the pathogenesis of Parkinson's disease (PD), but the underlying cause remains elusive. This work investigated the role of ALCAT1, an acyltransferase that catalyzes pathological remodeling of CL in various aging-related diseases, in a mouse model of PD induced by 1-methyl-4-phenyl-1,2,4,6-tetrahydropyridine (MPTP)...
March 5, 2019: Aging Cell
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