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https://www.readbyqxmd.com/read/28213406/mitochondria-regulated-formation-of-endothelial-extracellular-vesicles-shifts-the-mediator-of-flow-induced-vasodilation
#1
Julie K Freed, Matthew J Durand, Brian Robert Hoffmann, John C Densmore, Andrew S Greene, David D Gutterman
In order to examine the effect of endothelial-derived extracellular vesicles (eEVs) on the mechanism of flow-induced dilation (FID) composition, formation, and functional effects on the mechanism of FID were examined from two different eEV subtypes, one produced from ceramide, the other from plasminogen-activator inhibitor 1 (PAI-1). Using videomicroscopy, internal diameter changes in response to increases in flow were measured in human adipose resistance arteries acutely exposed (30min) to eEVs derived from cultured endothelial cells exposed to ceramide or PAI-1...
February 17, 2017: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/28213053/nerol-triggers-mitochondrial-dysfunction-and-disruption-via-elevation-of-ca-2-and-ros-in-candida-albicans
#2
Jun Tian, Zhaoqun Lu, Yanzhen Wang, Man Zhang, Xueyan Wang, Xudong Tang, Xue Peng, Hong Zeng
The antifungal activity of Nerol (NEL) against Candida albicans, a pathogenic fungus, has a minimum inhibitory concentration (MIC) of 4.4mM that causes noteworthy candidacidal activity through an apoptosis-like mechanism. Calcium (Ca(2+)) levels and reactive oxygen species (ROS) production, which are the major causes of apoptosis, were determined in C. albicans cells treated with NEL and were found to increase, which related to mitochondrial dysfunction and disruption. A series of characteristic changes of apoptosis caused by NEL, including mitochondrial membrane depolarization, cytochrome c (cyt c) release, and metacaspase activation were examined using a flow cytometer and Western blot...
February 14, 2017: International Journal of Biochemistry & Cell Biology
https://www.readbyqxmd.com/read/28211874/datf4-regulation-of-mitochondrial-folate-mediated-one-carbon-metabolism-is-neuroprotective
#3
Ivana Celardo, Susann Lehmann, Ana C Costa, Samantha Hy Loh, L Miguel Martins
Neurons rely on mitochondria as their preferred source of energy. Mutations in PINK1 and PARKIN cause neuronal death in early-onset Parkinson's disease (PD), thought to be due to mitochondrial dysfunction. In Drosophila pink1 and parkin mutants, mitochondrial defects lead to the compensatory upregulation of the mitochondrial one-carbon cycle metabolism genes by an unknown mechanism. Here we uncover that this branch is triggered by the activating transcription factor 4 (ATF4). We show that ATF4 regulates the expression of one-carbon metabolism genes SHMT2 and NMDMC as a protective response to mitochondrial toxicity...
February 17, 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28211814/are-major-dementias-triggered-by-poor-blood-flow-to-the-brain-theoretical-considerations
#4
Jack C de la Torre
There is growing evidence that chronic brain hypoperfusion plays a central role in the development of Alzheimer's disease (AD) long before dyscognitive symptoms or amyloid-β accumulation in the brain appear. This commentary proposes that dementia with Lewy bodies (DLB), frontotemporal dementia (FTD), and Creutzfeldt-Jakob disease (CJD) may also develop from chronic brain hypoperfusion following a similar but not identical neurometabolic breakdown as AD. The argument to support this conclusion is that chronic brain hypoperfusion, which is found at the early stages of the three dementias reviewed here, will reduce oxygen delivery and lower oxidative phosphorylation promoting a steady decline in the synthesis of the cell energy fuel adenosine triphosphate (ATP)...
February 15, 2017: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/28210902/deletion-of-mammalian-sterile-20-like-kinase-1-attenuates-neuronal-loss-and-improves-locomotor-function-in-a-mouse-model-of-spinal-cord-trauma
#5
Pan-Feng Wang, Da-Yuan Xu, Yuntong Zhang, Xiao-Bin Liu, Yan Xia, Pan-Yu Zhou, Qing-Ge Fu, Shuo-Gui Xu
Neuronal cell death following spinal cord injury (SCI) is an important contributor to neurological deficits. The purpose of our work was to delineate the function of mammalian sterile 20-like kinase 1 (Mst1), a pro-apoptotic kinase and key mediator of apoptotic signaling, in the pathogenesis of an experimental mouse model of SCI. Male mice received a mid-thoracic spinal contusion injury, and it was found that phosphorylation of Mst1 at the injured site was enhanced significantly following SCI. Furthermore, when compared to the wild-type controls, Mst1-deficient mice displayed improved locomotor function by increased Basso mouse scale score...
February 16, 2017: Molecular and Cellular Biochemistry
https://www.readbyqxmd.com/read/28209723/functional-metabolic-and-dynamic-mitochondrial-changes-in-the-rat-cirrhosis-hepatocellular-carcinoma-model-and-the-protective-effect-of-ifc-305
#6
Enrique Chavez, Maria Guadalupe Lozano-Rosas, Mariana Dominguez-Lopez, Gabriela Velasco-Loyden, Jesus Rafael Rodriguez-Aguilera, Concepcion Jose-Nunez, Marietta Tuena de Gomez-Puyou, Victoria Chagoya de Sanchez
BACKGROUND: Mitochondrion is an important metabolic and energetic organelle which regulates several cellular processes. Mitochondrial dysfunction has been related with liver diseases including hepatocellular carcinoma. As a result, the energetic demand is not properly supplied and mitochondrial morphologic changes has been observed resulting in an altered metabolism. We previously demonstrated the chemopreventive effect of the hepatoprotector IFC-305. AIM: In this work we aimed to evaluate the functional, metabolic, and dynamic mitochondrial alterations in the sequential model of cirrhosis-hepatocellular carcinoma induced by diethylnitrosamine in rats and the possible beneficial effect of IFC-305...
February 16, 2017: Journal of Pharmacology and Experimental Therapeutics
https://www.readbyqxmd.com/read/28209644/mitochondrial-dysfunction-induces-dendritic-loss-via-eif2%C3%AE-phosphorylation
#7
Taiichi Tsuyama, Asako Tsubouchi, Tadao Usui, Hiromi Imamura, Tadashi Uemura
Mitochondria are key contributors to the etiology of diseases associated with neuromuscular defects or neurodegeneration. How changes in cellular metabolism specifically impact neuronal intracellular processes and cause neuropathological events is still unclear. We here dissect the molecular mechanism by which mitochondrial dysfunction induced by Prel aberrant function mediates selective dendritic loss in Drosophila melanogaster class IV dendritic arborization neurons. Using in vivo ATP imaging, we found that neuronal cellular ATP levels during development are not correlated with the progression of dendritic loss...
February 16, 2017: Journal of Cell Biology
https://www.readbyqxmd.com/read/28208618/the-function-of-the-mitochondrial-calcium-uniporter-in-neurodegenerative-disorders
#8
REVIEW
Yajin Liao, Yuan Dong, Jinbo Cheng
The mitochondrial calcium uniporter (MCU)-a calcium uniporter on the inner membrane of mitochondria-controls the mitochondrial calcium uptake in normal and abnormal situations. Mitochondrial calcium is essential for the production of adenosine triphosphate (ATP); however, excessive calcium will induce mitochondrial dysfunction. Calcium homeostasis disruption and mitochondrial dysfunction is observed in many neurodegenerative disorders. However, the role and regulatory mechanism of the MCU in the development of these diseases are obscure...
February 10, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28208064/mitochondrial-genes-are-altered-in-blood-early-in-alzheimer-s-disease
#9
Katie Lunnon, Aoife Keohane, Ruth Pidsley, Stephen Newhouse, Joanna Riddoch-Contreras, Elisabeth B Thubron, Matthew Devall, Hikka Soininen, Iwona Kłoszewska, Patrizia Mecocci, Magda Tsolaki, Bruno Vellas, Leonard Schalkwyk, Richard Dobson, Afshan N Malik, John Powell, Simon Lovestone, Angela Hodges
Although mitochondrial dysfunction is a consistent feature of Alzheimer's disease in the brain and blood, the molecular mechanisms behind these phenomena are unknown. Here we have replicated our previous findings demonstrating reduced expression of nuclear-encoded oxidative phosphorylation (OXPHOS) subunits and subunits required for the translation of mitochondrial-encoded OXPHOS genes in blood from people with Alzheimer's disease and mild cognitive impairment. Interestingly this was accompanied by increased expression of some mitochondrial-encoded OXPHOS genes, namely those residing closest to the transcription start site of the polycistronic heavy chain mitochondrial transcript (MT-ND1, MT-ND2, MT-ATP6, MT-CO1, MT-CO2, MT-C03) and MT-ND6 transcribed from the light chain...
January 7, 2017: Neurobiology of Aging
https://www.readbyqxmd.com/read/28202582/dynamic-changes-in-cardiac-mitochondrial-metabolism-during-warm-acclimation-in-rainbow-trout
#10
Nicolas Pichaud, Andreas Ekström, Kim Hellgren, Erik Sandblom
Although the mitochondrial metabolism responses to warm acclimation have been widely studied in fish, the time course of this process is less understood. Here, we characterise changes of rainbow trout (Oncorhyncus mykiss) cardiac mitochondrial metabolism during acute warming from 10 to 16°C, and during the subsequent warm acclimation for 39 days (D). We repeatedly measured mitochondrial O2 consumption in cardiac permeabilized fibers and functional integrity of mitochondria (i.e. mitochondrial coupling and cytochrome c effect) at two assay temperatures (10 and 16°C), as well as citrate synthase (CS) and lactate dehydrogenase (LDH) activities at room temperature...
February 15, 2017: Journal of Experimental Biology
https://www.readbyqxmd.com/read/28199200/mitochondrial-dna-mitochondrial-dysfunction-and-cardiac-manifestations
#11
Sung Ryul Lee, Nari Kim, Yeun Hee Noh, Zhelong Xu, Kyung Soo Ko, Byoung Doo Rhee, Jin Han
Mitochondria, are the powerhouses of cells, have their own DNA (mtDNA), regulate the transport of metabolites and ions, and impact cell physiology, survival, and death. Mitochondrial dysfunction, including impaired oxidative phosphorylation, preferentially affects heart function due to an imbalance of energy supply and demand. Recently, mitochondrial mutations and associated mitochondrial dysfunction were suggested as a causal factor of cardiac manifestations. Oxidative stress largely influences mtDNA stability due to oxidative modifications of mtDNA...
March 1, 2017: Frontiers in Bioscience (Landmark Edition)
https://www.readbyqxmd.com/read/28199195/tissue-transglutaminase-tg2-and-mitochondrial-function-and-dysfunction
#12
Thung-S Lai, Cheng-Jui Lin, Yu-Ting Wu, Chih-Jen Wu
Mitochondria are the cell's power plant to satisfy the energy demands. However, dysfunctional mitochondria can cause overproduction of reactive oxygen species (ROS), oxidative stress, and alteration of calcium homeostasis, which are the hallmarks of mitochondrial diseases. Under prolong oxidative stress, repeated cytosolic calcium elevations even only transiently, can lead to activation of some enzymes. One calcium-activated enzyme with demonstrated pathophysiological important in mitochondrial disease is tissue transglutaminase (TG2)...
March 1, 2017: Frontiers in Bioscience (Landmark Edition)
https://www.readbyqxmd.com/read/28198506/inhibition-of-mitochondrial-calcium-uptake-1-in-drosophila-neurons
#13
P G M'Angale, B E Staveley
The mitochondrial calcium uptake 1 (MICU1) is a regulatory subunit of the mitochondrial calcium uniporter that plays an important role in calcium sensing. It contains two EF-hand domains that are well conserved across diverse species from protozoa to plants and metazoans. The loss of MICU1 function in mammals is attributed to several neurological disorders that involve movement dysfunction. The CG4495 gene in Drosophila melanogaster was identified as a putative homolog of MICU1 in the HomoloGene database of the National Centre for Biotechnology Information (NCBI)...
February 8, 2017: Genetics and Molecular Research: GMR
https://www.readbyqxmd.com/read/28194828/mitochondrial-dysfunction-and-ovarian-aging
#14
Tianren Wang, Man Zhang, Zongliang Jiang, Emre Seli
Mitochondria are double-membrane-bound organelles that are responsible for the generation of most of the cell's energy. Mitochondrial dysfunction has been implicated in cellular senescence in general and ovarian aging in particular. Recent studies exploited this association by studying mitochondrial DNA (mtDNA) copy number as a potential biomarker of embryo viability and the use of mitochondrial nutrients and autologous mitochondrial transfer as a potential treatment for poor ovarian function and response.
February 13, 2017: American Journal of Reproductive Immunology: AJRI
https://www.readbyqxmd.com/read/28194639/ultrafine-particulate-matter-increases-cardiac-ischemia-reperfusion-injury-via-mitochondrial-permeability-transition-pore
#15
Nathan A Holland, Chad R Fraiser, Ruben C Sloan, Robert B Devlin, David A Brown, Christopher J Wingard
Ultrafine particulate matter (UFP) has been associated with increased cardiovascular morbidity and mortality. However, the mechanisms that drive PM-associated cardiovascular disease and dysfunction remain unclear. We examined the impact of oropharyngeal aspiration of 100 μg UFP from the Chapel Hill, NC, air shed in Sprague-Dawley rats on cardiac function, arrhythmogenesis, and cardiac ischemia/reperfusion (I/R) injury using a Langendorff working heart model. We found that exposure to UFP was capable of significantly exacerbating cardiac I/R injury without changing overall cardiac function or major changes in arrhythmogenesis...
February 13, 2017: Cardiovascular Toxicology
https://www.readbyqxmd.com/read/28194437/mitochondrial-quality-control-dysregulation-in-conditional-ho-1-mice
#16
Hagir B Suliman, Jeffrey E Keenan, Claude A Piantadosi
The heme oxygenase-1 (Hmox1; HO-1) pathway was tested for defense of mitochondrial quality control in cardiomyocyte-specific Hmox1 KO mice (HO-1[CM](-/-)) exposed to oxidative stress (100% O2). After 48 hours of exposure, these mice showed persistent cardiac inflammation and oxidative tissue damage that caused sarcomeric disruption, cardiomyocyte death, left ventricular dysfunction, and cardiomyopathy, while control hearts showed minimal damage. After hyperoxia, HO-1(CM)(-/-) hearts showed suppression of the Pgc-1α/nuclear respiratory factor-1 (NRF-1) axis, swelling, low electron density mitochondria by electron microscopy (EM), increased cell death, and extensive collagen deposition...
February 9, 2017: JCI Insight
https://www.readbyqxmd.com/read/28193035/mitochondria-targeted-ratiometric-fluorescent-nanosensor-for-simultaneous-biosensing-and-imaging-of-o2-%C3%A2-and-ph-in-live-cells
#17
Hong Huang, Fangyuan Dong, Yang Tian
Intracellular pH undertakes critical functions in the formation of a proton gradient and electrochemical potential that drives the adenosine triphosphate synthesis. It is also involved in various metabolic processes occurring in mitochondria, such as the generation of reactive oxygen species, calcium regulation, as well as the triggering of cell proliferation and apoptosis. Meanwhile, the aberrant accumulation of O2(•-) within mitochondria is frequently intertwined with mitochondrial dysfunction and disease development...
December 20, 2016: Analytical Chemistry
https://www.readbyqxmd.com/read/28192238/molecular-networks-related-to-the-immune-system-and-mitochondria-are-targets-for-the-pesticide-dieldrin-in-the-zebrafish-danio-rerio-central-nervous-system
#18
Andrew M Cowie, Kathleena I Sarty, Angella Mercer, Jin Koh, Karen A Kidd, Christopher J Martyniuk
: The objectives of this study were to determine the behavioral and molecular responses in the adult zebrafish (Danio rerio) central nervous system (CNS) following a dietary exposure to the pesticide dieldrin. Zebrafish were fed pellets spiked with 0.03, 0.15, or 1.8μg/g dieldrin for 21days. Behavioral analysis revealed no difference in exploratory behaviors or those related to anxiety. Transcriptional networks for T-cell aggregation and selection were decreased in expression suggesting an immunosuppressive effect of dieldrin, consistent with other studies investigating organochlorine pesticides...
February 9, 2017: Journal of Proteomics
https://www.readbyqxmd.com/read/28190529/mitophagy-and-alzheimer-s-disease-cellular-and-molecular-mechanisms
#19
REVIEW
Jesse S Kerr, Bryan A Adriaanse, Nigel H Greig, Mark P Mattson, M Zameel Cader, Vilhelm A Bohr, Evandro F Fang
Neurons affected in Alzheimer's disease (AD) experience mitochondrial dysfunction and a bioenergetic deficit that occurs early and promotes the disease-defining amyloid beta peptide (Aβ) and Tau pathologies. Emerging findings suggest that the autophagy/lysosome pathway that removes damaged mitochondria (mitophagy) is also compromised in AD, resulting in the accumulation of dysfunctional mitochondria. Results in animal and cellular models of AD and in patients with sporadic late-onset AD suggest that impaired mitophagy contributes to synaptic dysfunction and cognitive deficits by triggering Aβ and Tau accumulation through increases in oxidative damage and cellular energy deficits; these, in turn, impair mitophagy...
February 9, 2017: Trends in Neurosciences
https://www.readbyqxmd.com/read/28188904/exposure-to-cadmium-during-in-vitro-maturation-at-environmental-nanomolar-levels-impairs-oocyte-fertilization-through-oxidative-damage-a-large-animal-model-study
#20
N A Martino, G Marzano, M Mangiacotti, O Miedico, A M Sardanelli, A Gnoni, G M Lacalandra, A E Chiaravalle, E Ciani, L Bogliolo, F Minervini, F Pizzi, M E Dell'Aquila
Cadmium is a highly toxic heavy metal with negative effects on oocyte fertilization. The aim of this study was to analyse whether cadmium-induced impairment of fertilization is caused by mitochondria dysfunction and oxidative stress in the cumulus-oocyte complex (COC). Preliminarily, 19 trace element levels were measured in ovaries from juvenile and adult ewes and age-related cadmium ovarian bioaccumulation at nanomolar concentrations was found. COCs from juvenile and adult ewes, exposed during in vitro maturation to 1nM or 100nM CdCl2, and subjected to in vitro fertilization showed significantly lower fertilization rates in exposed COCs compared with controls...
February 7, 2017: Reproductive Toxicology
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