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Mitochondria cell differentiation

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https://www.readbyqxmd.com/read/27901621/perfluorooctanoic-acid-induces-mitochondrial-dysfunction-in-mc3t3-e1-osteoblast-cells
#1
Eun Mi Choi, Kwang Sik Suh, Sang Youl Rhee, Seungjoon Oh, Jeong-Taek Woo, Sung Woon Kim, Young Seol Kim, Youngmi Kim Pak, Suk Chon
Perfluorooctanoic acid (PFOA), a stable organic perfluorinated compound, is an emerging persistent organic pollutant, found widely in human and wildlife populations. Recent evidence suggests that exposure to environmental toxicants can be associated with higher risks of osteoporosis and fractures. We studied the cellular toxicology of PFOA in MC3T3-E1osteoblast cells. To examine the effect of PFOA, we measured cell viability, reactive oxygen species (ROS), mitochondrial superoxide, and mitochondrial parameters including adenosine triphosphate (ATP) level, mitochondrial membrane potential (MMP), cardiolipin content, and cytochrome c release in MC3T3-E1 cells...
November 30, 2016: Journal of Environmental Science and Health. Part A, Toxic/hazardous Substances & Environmental Engineering
https://www.readbyqxmd.com/read/27896136/attention-deficit-hyperactivity-disorder-suffers-from-mitochondrial-dysfunction
#2
Poonam Verma, Alpana Singh, Dominic Ngima Nthenge-Ngumbau, Usha Rajamma, Swagata Sinha, Kanchan Mukhopadhyay, Kochupurackal P Mohanakumar
BACKGROUND: Pathophysiology of attention-deficit hyperactivity disorder (ADHD) is not known, and therefore the present study investigated mitochondrial defects, if any in cybrids created from patients and control population. METHODS: To investigate mitochondrial pathology in ADHD, cybrids cell lines were created from ADHD probands and controls by fusing their platelets with ρ(0)-cells prepared from SH-SY5Y neuroblastoma cell line. Cellular respiration, oxidative stress, mitochondrial membrane potential and morphology were evaluated employing oxygraph, mitochondria-specific fluorescence staining and evaluation by FACS, and immunocytochemistry...
December 2016: BBA Clinical
https://www.readbyqxmd.com/read/27866262/impairment-of-mitochondria-dynamics-by-human-a53t-%C3%AE-synuclein-and-rescue-by-nap-davunetide-in-a-cell-model-for-parkinson-s-disease
#3
T Q Melo, K C van Zomeren, M F R Ferrari, H W G M Boddeke, J C V M Copray
The formation of oligomers and aggregates of overexpressed or mutant α-synuclein play a role in the degeneration of dopaminergic neurons in Parkinson's disease by causing dysfunction of mitochondria, reflected in their disturbed mobility and production of ROS. The mode of action and mechanisms underlying this mitochondrial impairment is still unclear. We have induced stable expression of wild-type, A30P or A53T α-synuclein in neuronally differentiated SH-SY5Y neuroblastoma cells and studied anterograde and retrograde mitochondrial trafficking in this cell model for Parkinson's disease...
November 19, 2016: Experimental Brain Research. Experimentelle Hirnforschung. Expérimentation Cérébrale
https://www.readbyqxmd.com/read/27861613/non-serotonergic-neurotoxicity-by-mdma-ecstasy-in-neurons-derived-from-mouse-p19-embryonal-carcinoma-cells
#4
Dina Popova, Andréas Forsblad, Sanaz Hashemian, Stig O P Jacobsson
3,4-methylenedioxymethamphetamine (MDMA; ecstasy) is a commonly abused recreational drug that causes neurotoxic effects in both humans and animals. The mechanism behind MDMA-induced neurotoxicity is suggested to be species-dependent and needs to be further investigated on the cellular level. In this study, the effects of MDMA in neuronally differentiated P19 mouse embryonal carcinoma cells have been examined. MDMA produces a concentration-, time- and temperature-dependent toxicity in differentiated P19 neurons, as measured by intracellular MTT reduction and extracellular LDH activity assays...
2016: PloS One
https://www.readbyqxmd.com/read/27859413/zak%C3%AE-antagonizes-and-ameliorates-the-cardiac-hypertrophic-and-apoptotic-effects-induced-by-zak%C3%AE
#5
Chien-Yao Fu, Wei-Wen Kuo, Tsung-Jung Ho, Su-Ying Wen, Ling-Chun Lin, Yan-Shen Tseng, Hui-Chuan Hung, Vijaya Padma Viswanadha, Jaw-Ji Yang, Chih-Yang Huang
ZAK (sterile alpha motif and leucine zipper containing kinase AZK), a serine/threonine kinase with multiple biochemical functions, has been associated with various cell processes, including cell proliferation, cell differentiation, and cardiac hypertrophy. In our previous reports, we found that the activation of ZAKα signaling was critical for cardiac hypertrophy. In this study, we show that the expression of ZAKα activated apoptosis through both a FAS-dependent pathway and a mitochondria-dependent pathway by subsequently inducing caspase-3...
November 16, 2016: Cell Biochemistry and Function
https://www.readbyqxmd.com/read/27859025/modeling-drug-induced-neuropathy-using-human-ipscs-for-predictive-toxicology
#6
Ryo Ohara, Keiko Imamura, Fukiko Morii, Naohiro Egawa, Kayoko Tsukita, Takako Enami, Ran Shibukawa, Toshiki Mizuno, Masanori Nakagawa, Haruhisa Inoue
Drugs under development can cause unpredicted toxicity in humans due to differential drug responsiveness between humans and other disease models, resulting in clinical trial failures. Human induced pluripotent stem cells (iPSCs) are expected to represent a useful tool for toxicity testing. However, among many assays, appropriate cellular assays for predicting neurotoxicity in an iPSC-based model are still uncertain. Here, we generated neurons from iPSCs of Charcot-Marie-Tooth disease (CMT) patients, who are sensitive to anti-cancer drugs and present with the adverse reaction of neuropathy, and analyzed cellular phenotypes...
November 9, 2016: Clinical Pharmacology and Therapeutics
https://www.readbyqxmd.com/read/27854030/simple-oxygraphic-analysis-for-the-presence-of-adenylate-kinase-1-and-2-in-normal-and-tumor-cells
#7
Aleksandr Klepinin, Lyudmila Ounpuu, Rita Guzun, Vladimir Chekulayev, Natalja Timohhina, Kersti Tepp, Igor Shevchuk, Uwe Schlattner, Tuuli Kaambre
The adenylate kinase (AK) isoforms network plays an important role in the intracellular energy transfer processes, the maintenance of energy homeostasis, and it is a major player in AMP metabolic signaling circuits in some highly-differentiated cells. For this purpose, a rapid and sensitive method was developed that enables to estimate directly and semi-quantitatively the distribution between cytosolic AK1 and mitochondrial AK2 localized in the intermembrane space, both in isolated cells and tissue samples (biopsy material)...
November 17, 2016: Journal of Bioenergetics and Biomembranes
https://www.readbyqxmd.com/read/27852805/computational-properties-of-mitochondria-in-t-cell-activation-and-fate
#8
REVIEW
Roman Uzhachenko, Anil Shanker, Geneviève Dupont
In this article, we review how mitochondrial Ca(2+) transport (mitochondrial Ca(2+) uptake and Na(+)/Ca(2+) exchange) is involved in T cell biology, including activation and differentiation through shaping cellular Ca(2+) signals. Based on recent observations, we propose that the Ca(2+) crosstalk between mitochondria, endoplasmic reticulum and cytoplasm may form a proportional-integral-derivative (PID) controller. This PID mechanism (which is well known in engineering) could be responsible for computing cellular decisions...
November 2016: Open Biology
https://www.readbyqxmd.com/read/27851770/direct-stimulation-of-islet-insulin-secretion-by-glycolytic-and-mitochondrial-metabolites-in-kcl-depolarized-islets
#9
Javier Pizarro-Delgado, Jude T Deeney, Barbara E Corkey, Jorge Tamarit-Rodriguez
We have previously demonstrated that islet depolarization with 70 mM KCl opens Cx36 hemichannels and allows diffusion of small metabolites and cofactors through the β-cell plasma membrane. We have investigated in this islet "permeabilized" model whether glycolytic and citric acid cycle intermediates stimulate insulin secretion and how it correlates with ATP production (islet content plus extracellular nucleotide accumulation). Glycolytic intermediates (10 mM) stimulated insulin secretion and ATP production similarly...
2016: PloS One
https://www.readbyqxmd.com/read/27843711/iron-overload-induced-death-of-osteoblasts-in-vitro-involvement-of-the-mitochondrial-apoptotic-pathway
#10
Qing Tian, Shilei Wu, Zhipeng Dai, Jingjing Yang, Jin Zheng, Qixin Zheng, Yong Liu
BACKGROUND: Iron overload is recognized as a new pathogenfor osteoporosis. Various studies demonstrated that iron overload could induce apoptosis in osteoblasts and osteoporosis in vivo. However, the exact molecular mechanisms involved in the iron overload-mediated induction of apoptosis in osteoblasts has not been explored. PURPOSE: In this study, we attempted to determine whether the mitochondrial apoptotic pathway is involved in iron-induced osteoblastic cell death and to investigate the beneficial effect of N-acetyl-cysteine (NAC) in iron-induced cytotoxicity...
2016: PeerJ
https://www.readbyqxmd.com/read/27834956/a-bak-dependent-mitochondrial-amplification-step-contributes-to-smac-mimetic-glucocorticoid-induced-necroptosis
#11
Katharina Rohde, Lara Kleinesudeik, Stefanie Roesler, Oliver Löwe, Juliana Heidler, Katrin Schröder, Ilka Wittig, Stefan Dröse, Simone Fulda
Necroptosis is a form of programmed cell death that critically depends on RIP3 and MLKL. However, the contribution of mitochondria to necroptosis is still poorly understood. In the present study, we discovered that mitochondrial perturbations play a critical role in Smac mimetic/Dexamethasone (Dexa)-induced necroptosis independently of death receptor ligands. We demonstrate that the Smac mimetic BV6 and Dexa cooperate to trigger necroptotic cell death in acute lymphoblastic leukemia (ALL) cells that are deficient in caspase activation due to absent caspase-8 expression or pharmacological inhibition by the caspase inhibitor zVAD...
November 11, 2016: Cell Death and Differentiation
https://www.readbyqxmd.com/read/27834955/mitochondria-mediate-cell-membrane-repair-and-contribute-to-duchenne-muscular-dystrophy
#12
Maria C Vila, Sree Rayavarapu, Marshall W Hogarth, Jack H Van der Meulen, Adam Horn, Aurelia Defour, Shin'ichi Takeda, Kristy J Brown, Yetrib Hathout, Kanneboyina Nagaraju, Jyoti K Jaiswal
Dystrophin deficiency is the genetic basis for Duchenne muscular dystrophy (DMD), but the cellular basis of progressive myofiber death in DMD is not fully understood. Using two dystrophin-deficient mdx mouse models, we find that the mitochondrial dysfunction is among the earliest cellular deficits of mdx muscles. Mitochondria in dystrophic myofibers also respond poorly to sarcolemmal injury. These mitochondrial deficits reduce the ability of dystrophic muscle cell membranes to repair and are associated with a compensatory increase in dysferlin-mediated membrane repair proteins...
November 11, 2016: Cell Death and Differentiation
https://www.readbyqxmd.com/read/27832395/mitoluhmes-an-engineered-neuronal-cell-line-for-the-analysis-of-the-motility-of-mitochondria
#13
Tomasz M Stępkowski, Sylwia Męczyńska-Wielgosz, Marcin Kruszewski
Perturbations in the transport of mitochondria and their quality control in neuronal cells underlie many types of neurological pathologies, whereas systems enabling convenient analysis of mitochondria behavior in cellular models of neurodegenerative diseases are limited. In this study, we present a modified version of lund human mesencephalic cells, mitoLUHMES, expressing GFP and mitochondrially targeted DsRed2 fluorescent proteins, intended for in vitro analysis of mitochondria trafficking by real-time fluorescence microscopy...
November 10, 2016: Cellular and Molecular Neurobiology
https://www.readbyqxmd.com/read/27821326/effects-of-transgenic-methionine-sulfoxide-reductase-a-msra-expression-on-lifespan-and-age-dependent-changes-in-metabolic-function-in-mice
#14
Adam B Salmon, Geumsoo Kim, Chengyu Liu, Jonathan D Wren, Constantin Georgescu, Arlan Richardson, Rodney L Levine
Mechanisms that preserve and maintain the cellular proteome are associated with long life and healthy aging. Oxidative damage is a significant contributor to perturbation of proteostasis and is dealt with by the cell through regulation of antioxidants, protein degradation, and repair of oxidized amino acids. Methionine sulfoxide reductase A (MsrA) repairs oxidation of free- and protein-bound methionine residues through enzymatic reduction and is found in both the cytosol and the mitochondria. Previous studies in Drosophila have shown that increasing expression of MsrA can extend longevity...
December 2016: Redox Biology
https://www.readbyqxmd.com/read/27818678/transcriptome-wide-analysis-reveals-the-role-of-ppar%C3%AE-controlling-the-lipid-metabolism-in-goat-mammary-epithelial-cells
#15
Hengbo Shi, Wangsheng Zhao, Changhui Zhang, Khuram Shahzad, Jun Luo, Juan J Loor
To explore the large-scale effect of peroxisome proliferator-activated receptor γ (PPARG) in goat mammary epithelial cells (GMEC), an oligonucleotide microarray platform was used for transcriptome profiling in cells overexpressing PPARG and incubated with or without rosiglitazone (ROSI, a PPARγ agonist). A total of 1143 differentially expressed genes (DEG) due to treatment were detected. The Dynamic Impact Approach (DIA) analysis uncovered the most impacted and induced pathways "fatty acid elongation in mitochondria," "glycosaminoglycan biosynthesis-keratan sulfate," and "pentose phosphate pathway...
2016: PPAR Research
https://www.readbyqxmd.com/read/27815330/plants-grow-with-a-little-help-from-their-organelle-friends
#16
REVIEW
Judith Van Dingenen, Jonas Blomme, Nathalie Gonzalez, Dirk Inzé
Chloroplasts and mitochondria are indispensable for plant development. They not only provide energy and carbon sources to cells, but also have evolved to become major players in a variety of processes such as amino acid metabolism, hormone biosynthesis and cellular signalling. As semi-autonomous organelles, they contain a small genome that relies largely on nuclear factors for its maintenance and expression. An intensive crosstalk between the nucleus and the organelles is therefore essential to ensure proper functioning, and the nuclear genes encoding organellar proteins involved in photosynthesis and oxidative phosphorylation are obviously crucial for plant growth...
November 4, 2016: Journal of Experimental Botany
https://www.readbyqxmd.com/read/27815210/function-of-cyp11a1-in-the-mitochondria
#17
Yu Chien, Karen Rosal, Bon-Chu Chung
Steroids are synthesized from the adrenal glands and gonads by enzymes of the cytochromes P450 and hydroxysteroid dehydrogenase in nature. These enzymes are located in the membrane of endoplasmic reticulum and mitochondria to catalyze redox reactions using electrons transported from the membrane. In the mitochondria, steroidogenic enzymes are inserted into the inner membrane with the bulk of the protein facing the matrix. They are not only important for steroid biosynthesis, their presence also affects mitochondrial morphology...
November 1, 2016: Molecular and Cellular Endocrinology
https://www.readbyqxmd.com/read/27810911/the-mitochondrial-protein-chchd2-primes-the-differentiation-potential-of-human-induced-pluripotent-stem-cells-to-neuroectodermal-lineages
#18
Lili Zhu, Aurora Gomez-Duran, Gabriele Saretzki, Shibo Jin, Katarzyna Tilgner, Dario Melguizo-Sanchis, Georgios Anyfantis, Jumana Al-Aama, Ludovic Vallier, Patrick Chinnery, Majlinda Lako, Lyle Armstrong
Human induced pluripotent stem cell (hiPSC) utility is limited by variations in the ability of these cells to undergo lineage-specific differentiation. We have undertaken a transcriptional comparison of human embryonic stem cell (hESC) lines and hiPSC lines and have shown that hiPSCs are inferior in their ability to undergo neuroectodermal differentiation. Among the differentially expressed candidates between hESCs and hiPSCs, we identified a mitochondrial protein, CHCHD2, whose expression seems to correlate with neuroectodermal differentiation potential of pluripotent stem cells...
October 24, 2016: Journal of Cell Biology
https://www.readbyqxmd.com/read/27808250/mtorc1-inhibitor-rapamycin-and-er-stressor-tunicamycin-induce-differential-patterns-of-er-mitochondria-coupling
#19
Roberto Bravo-Sagua, Camila López-Crisosto, Valentina Parra, Marcelo Rodriguez-Peña, Beverly A Rothermel, Andrew F G Quest, Sergio Lavandero
Efficient mitochondrial Ca(2+) uptake takes place at contact points between the ER and mitochondria, and represents a key regulator of many cell functions. In a previous study with HeLa cells, we showed that ER-to-mitochondria Ca(2+) transfer increases during the early phase of ER stress induced by tunicamycin as an adaptive response to stimulate mitochondrial bioenergetics. It remains unknown whether other types of stress signals trigger similar responses. Here we observed that rapamycin, which inhibits the nutrient-sensing complex mTORC1, increased ER-mitochondria coupling in HeLa cells to a similar extent as did tunicamycin...
November 3, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27802911/mitochondrial-multifaceted-dysfunction-in-schizophrenia-complex-i-as-a-possible-pathological-target
#20
REVIEW
Dorit Ben-Shachar
Mitochondria are key players in various essential cellular processes beyond being the main energy supplier of the cell. Accordingly, they are involved in neuronal synaptic transmission, neuronal growth and sprouting and consequently neuronal plasticity and connectivity. In addition, mitochondria participate in the modulation of gene transcription and inflammation as well in physiological responses in health and disease. Schizophrenia is currently regarded as a neurodevelopmental disorder associated with impaired immune system, aberrant neuronal differentiation and abnormalities in various neurotransmitter systems mainly the dopaminergic, glutaminergic and GABAergic...
October 29, 2016: Schizophrenia Research
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