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Mitochondria cell differentiation

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https://www.readbyqxmd.com/read/28220896/mitochondrial-dysregulation-secondary-to-endoplasmic-reticulum-stress-in-autosomal-dominant-tubulointerstitial-kidney-disease-umod-adtkd-umod
#1
Elisabeth Kemter, Thomas Fröhlich, Georg J Arnold, Eckhard Wolf, Rüdiger Wanke
'Autosomal dominant tubulointerstitial kidney disease - UMOD' (ADTKD-UMOD) is caused by impaired maturation and secretion of mutant uromodulin (UMOD) in thick ascending limb of Henle loop (TAL) cells, resulting in endoplasmic reticulum (ER) stress and unfolded protein response (UPR). To gain insight into pathophysiology, we analysed proteome profiles of TAL-enriched outer renal medulla samples from ADTKD-UMOD and control mice by quantitative LC-MS/MS. In total, 212 differentially abundant proteins were identified...
February 21, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28219123/identification-of-core-gene-networks-and-hub-genes-associated-with-progression-of-nonalcoholic-fatty-liver-disease-by-rna-sequencing
#2
Kikuko Hotta, Masataka Kikuchi, Takuya Kitamoto, Aya Kitamoto, Yuji Ogawa, Yasushi Honda, Takaomi Kessoku, Kaori Kobayashi, Masato Yoneda, Kento Imajo, Wataru Tomeno, Akihiro Nakaya, Yutaka Suzuki, Satoru Saito, Atsushi Nakajima
AIM: Nonalcoholic fatty liver disease (NAFLD) progresses because of the interaction between numerous genes. Thus, we performed weighted gene co-expression network analysis to identify core gene networks and key genes associated with NAFLD progression. METHODS: We enrolled 39 patients with mild NAFLD (fibrosis stages 0 to 2) and 21 with advanced NAFLD (fibrosis stages 3 or 4). Total RNA was extracted from frozen liver biopsies, and sequenced to capture a large dynamic range of expression levels...
February 20, 2017: Hepatology Research: the Official Journal of the Japan Society of Hepatology
https://www.readbyqxmd.com/read/28216144/patient-ipsc-derived-neurons-for-disease-modeling-of-frontotemporal-dementia-with-mutation-in-chmp2b
#3
Yu Zhang, Benjamin Schmid, Nanett K Nikolaisen, Mikkel A Rasmussen, Blanca I Aldana, Mikkel Agger, Kirstine Calloe, Tina C Stummann, Hjalte M Larsen, Troels T Nielsen, Jinrong Huang, Fengping Xu, Xin Liu, Lars Bolund, Morten Meyer, Lasse K Bak, Helle S Waagepetersen, Yonglun Luo, Jørgen E Nielsen, Bjørn Holst, Christian Clausen, Poul Hyttel, Kristine K Freude
The truncated mutant form of the charged multivesicular body protein 2B (CHMP2B) is causative for frontotemporal dementia linked to chromosome 3 (FTD3). CHMP2B is a constituent of the endosomal sorting complex required for transport (ESCRT) and, when mutated, disrupts endosome-to-lysosome trafficking and substrate degradation. To understand the underlying molecular pathology, FTD3 patient induced pluripotent stem cells (iPSCs) were differentiated into forebrain-type cortical neurons. FTD3 neurons exhibited abnormal endosomes, as previously shown in patients...
February 6, 2017: Stem Cell Reports
https://www.readbyqxmd.com/read/28211874/datf4-regulation-of-mitochondrial-folate-mediated-one-carbon-metabolism-is-neuroprotective
#4
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/28209995/rna-seq-based-transcriptomic-and-metabolomic-analysis-reveal-stress-responses-and-programmed-cell-death-induced-by-acetic-acid-in-saccharomyces-cerevisiae
#5
Yachen Dong, Jingjin Hu, Linlin Fan, Qihe Chen
As a typical harmful inhibitor in cellulosic hydrolyzates, acetic acid not only hinders bioethanol production, but also induces cell death in Saccharomyces cerevisiae. Herein, we conducted both transcriptomic and metabolomic analyses to investigate the global responses under acetic acid stress at different stages. There were 295 up-regulated and 427 down-regulated genes identified at more than two time points during acetic acid treatment (150 mM, pH 3.0). These differentially expressed genes (DEGs) were mainly involved in intracellular homeostasis, central metabolic pathway, transcription regulation, protein folding and stabilization, ubiquitin-dependent protein catabolic process, vesicle-mediated transport, protein synthesis, MAPK signaling pathways, cell cycle, programmed cell death, etc...
February 17, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28202400/protective-role-of-mitochondrial-peroxiredoxin-iii-against-uvb-induced-apoptosis-of-epidermal-keratinocytes
#6
Jin Young Baek, Sujin Park, Jiyoung Park, Ji Yong Jang, Su Bin Wang, Sin Ri Kim, Hyun Ae Woo, Kyung Min Lim, Tong-Shin Chang
Ultraviolet B (UVB) light induces generation of reactive oxygen species (ROS), ultimately leading to skin cell damage. Mitochondria are a major source of ROS in UVB-irradiated skin cells, with increased levels of mitochondrial ROS having been implicated in keratinocyte apoptosis. Peroxiredoxin III (PrxIII) is the most abundant and potent H2O2-removing enzyme in the mitochondria of most cell types. Here, the protective role of PrxIII against UVB-induced apoptosis of epidermal keratinocytes was investigated. Mitochondrial H2O2 levels were differentiated from other types of ROS using mitochondria-specific fluorescent H2O2 indicators...
February 12, 2017: Journal of Investigative Dermatology
https://www.readbyqxmd.com/read/28195557/biogenetic-and-morphofunctional-heterogeneity-of-mitochondria-the-case-of-synaptic-mitochondria
#7
Sergei V Fedorovich, Tatyana V Waseem, Ludmila V Puchkova
The mitochondria of different cells are different in their morphological and biochemical properties. These organelles generate free radicals during activity, leading inevitably to mitochondrial DNA damage. It is not clear how this problem is addressed in long-lived cells, such as neurons. We propose the hypothesis that mitochondria within the same cell also differ in lifespan and ability to divide. According to our suggestion, cells have a pool of 'stem' mitochondria with low metabolic activity and a pool of 'differentiated' mitochondria with significantly shorter lifespans and high metabolic activity...
February 14, 2017: Reviews in the Neurosciences
https://www.readbyqxmd.com/read/28194429/intracellular-assessment-of-atp-levels-in-caenorhabditis-elegans
#8
Konstantinos Palikaras, Nektarios Tavernarakis
Eukaryotic cells heavily depend on adenosine triphosphate (ATP) generated by oxidative phosphorylation (OXPHOS) within mitochondria. ATP is the major energy currency molecule, which fuels cell to carry out numerous processes, including growth, differentiation, transportation and cell death among others (Khakh and Burnstock, 2009). Therefore, ATP levels can serve as a metabolic gauge for cellular homeostasis and survival (Artal-Sanz and Tavernarakis, 2009; Gomes et al., 2011; Palikaras et al., 2015). In this protocol, we describe a method for the determination of intracellular ATP levels using a bioluminescence approach in the nematode Caenorhabditis elegans...
December 5, 2016: Bio-protocol
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
#9
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/28188219/distinct-effects-of-mir-210-reduction-on-neurogenesis-increased-neuronal-survival-of-inflammation-but-reduced-proliferation-associated-with-mitochondrial-enhancement
#10
Ludmila A Voloboueva, Xiaoyun Sun, Lijun Xu, Yi-Bing Ouyang, Rona G Giffard
Neurogenesis is essential to brain development, and plays a central role in the response to brain injury. Stroke and head trauma stimulate proliferation of endogenous neural stem cells (NSC). However, the survival of young neurons is sharply reduced by post-injury inflammation. Cellular mitochondria are critical to successful neurogenesis and are a major target of inflammatory injury. Mitochondrial protection was shown to improve survival of young neurons. This study tested whether reducing cellular microRNA-210 (miR-210) would enhance mitochondrial function and improve survival of young murine neurons under inflammatory conditions...
February 10, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/28183804/reduced-mitochondrial-activity-in-colonocytes-facilitates-ampk%C3%AE-2-dependent-inflammation
#11
Sandra Heller, Harrison M Penrose, Chloe Cable, Debjani Biswas, Hani Nakhoul, Melody Baddoo, Erik Flemington, Susan E Crawford, Suzana D Savkovic
Intestinal inflammation is associated with low levels of mucosal ATP, highlighting the importance of mitochondrial function associated with ATP production in the pathophysiology of the disease. In the inflamed colon of humans and mice, we found decreased levels of mitochondrial complex cytochrome c oxidase I/IV and lower ATP levels. Thus, we generated colonic ρ(0) cells with reduced mitochondrial function linked to ATP production by selective depletion of mitochondrial DNA. In these cells, RNA sequencing revealed a substantial number of differentially expressed transcripts, among which 240 belonged to inflammatory pathways activated in human inflamed colon and TNF-α-treated cells (false discovery rate < 0...
February 9, 2017: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/28181922/burn-serum-stimulates-myoblast-cell-death-associated-with-il-6-induced-mitochondrial-fragmentation
#12
Alvand Sehat, Ryan M Huebinger, Deborah L Carlson, Qun S Zang, Steven E Wolf, Juquan Song
BACKGROUND: Burn patients suffer muscle mass loss associated with hyperinflammation and hypercatabolism. The mitochondria are affected by this metabolic alteration. Mitochondrial fission activates a caspase cascade which ultimately leads to cell death. We postulate that burn-induced muscle loss is associated with increased mitochondrial fission and subsequent functional impairment. Further, we investigated whether the cytokine IL-6 plays a major role in mitochondrial fission-associated cell death after burn...
February 8, 2017: Shock
https://www.readbyqxmd.com/read/28167264/surface-modified-particles-loaded-with-camkii-inhibitor-protect-cardiac-cells-against-mitochondrial-injury
#13
Amaraporn Wongrakpanich, Angie S Morris, Sean M Geary, Mei-Ling A Joiner, Aliasger K Salem
An excess of calcium (Ca(2+)) influx into mitochondria during mitochondrial re-energization is one of the causes of myocardial cell death during ischemic/reperfusion injury. This overload of Ca(2+) triggers the mitochondrial permeability transition pore (mPTP) opening which leads to programmed cell death. During the ischemic/reperfusion stage, the activated Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) enzyme is responsible for Ca(2+) influx. To reduce CaMKII-related cell death, sub-micron particles composed of poly(lactic-co-glycolic acid) (PLGA), loaded with a CaMKII inhibitor peptide were fabricated...
February 3, 2017: International Journal of Pharmaceutics
https://www.readbyqxmd.com/read/28167126/mitochondrial-t3-receptor-and-targets
#14
Chantal Wrutniak-Cabello, François Casas, Gérard Cabello
The demonstration that TRα1 mRNA encodes a nuclear thyroid hormone receptor and two proteins imported into mitochondria with molecular masses of 43 and 28 KDa has brought new clues to better understand the pleiotropic influence of iodinated hormones. If p28 activity remains unknown, p43 binds to T3 responsive elements occurring in the organelle genome, and, in the T3 presence, stimulates mitochondrial transcription and the subsequent synthesis of mitochondrial encoded proteins. This influence increases mitochondrial activity and through changes in the mitochondrial/nuclear crosstalk affects important nuclear target genes regulating cell proliferation and differentiation, oncogenesis, or apoptosis...
February 3, 2017: Molecular and Cellular Endocrinology
https://www.readbyqxmd.com/read/28166796/coenzyme-q10-partially-restores-pathological-alterations-in-a-macrophage-model-of-gaucher-disease
#15
Mario de la Mata, David Cotán, Manuel Oropesa-Ávila, Marina Villanueva-Paz, Isabel de Lavera, Mónica Álvarez-Córdoba, Raquel Luzón-Hidalgo, Juan M Suárez-Rivero, Gustavo Tiscornia, José A Sánchez-Alcázar
BACKGROUND: Gaucher disease (GD) is caused by mutations in the GBA1 gene which encodes lysosomal β-glucocerebrosidase (GCase). In GD, partial or complete loss of GCase activity causes the accumulation of the glycolipids glucosylceramide (GlcCer) and glucosylsphingosine in the lysosomes of macrophages. In this manuscript, we investigated the effects of glycolipids accumulation on lysosomal and mitochondrial function, inflammasome activation and efferocytosis capacity in a THP-1 macrophage model of Gaucher disease...
February 6, 2017: Orphanet Journal of Rare Diseases
https://www.readbyqxmd.com/read/28164768/protective-effect-of-aspirin-against-oligomeric-a%C3%AE-42-induced-mitochondrial-alterations-and-neurotoxicity-in-differentiated-ec-p19-neuronal-cells
#16
Hamendra Singh Parmar, Zbynek Houdek, Martin Pesta, Vaclava Cerna, Pavel Dvorak, Jiri Hatina
Amyloid-beta (Aβ) induced mitochondrial dysfunction is one of the major causes of neuronal toxicity in Alzheimer's disease. Many recent reports suggest involvement of mitochondrial alterations through intracellular accumulation of oligomeric Aβ. These mitochondrial alterations include increased reactive oxygen species (ROS), mt-DNA depletion, decreased oxidative phosphorylation and ATP production, membrane depolarization, reduced number of mitochondria etc. These all defects cumulatively caused neural toxicity and alterations in cellular energy homeostasis...
February 2, 2017: Current Alzheimer Research
https://www.readbyqxmd.com/read/28158302/host-cell-interactions-of-outer-membrane-vesicle-associated-virulence-factors-of-enterohemorrhagic-escherichia-coli-o157-intracellular-delivery-trafficking-and-mechanisms-of-cell-injury
#17
Martina Bielaszewska, Christian Rüter, Andreas Bauwens, Lilo Greune, Kevin-André Jarosch, Daniel Steil, Wenlan Zhang, Xiaohua He, Roland Lloubes, Angelika Fruth, Kwang Sik Kim, M Alexander Schmidt, Ulrich Dobrindt, Alexander Mellmann, Helge Karch
Outer membrane vesicles (OMVs) are important tools in bacterial virulence but their role in the pathogenesis of infections caused by enterohemorrhagic Escherichia coli (EHEC) O157, the leading cause of life-threatening hemolytic uremic syndrome, is poorly understood. Using proteomics, electron and confocal laser scanning microscopy, immunoblotting, and bioassays, we investigated OMVs secreted by EHEC O157 clinical isolates for virulence factors cargoes, interactions with pathogenetically relevant human cells, and mechanisms of cell injury...
February 2017: PLoS Pathogens
https://www.readbyqxmd.com/read/28148493/subfunctionalization-of-cox4-paralogs-in-fish
#18
Danielle Porplycia, Gigi Y Lau, Jared McDonald, Zhilin Chen, Jeffrey G Richards, Christopher D Moyes
Cytochrome c oxidase (COX) subunit 4 has two paralogs in most vertebrates. The mammalian COX4-2 gene is hypoxia responsive and the protein has a disrupted ATP-binding site that confers kinetic properties on COX that distinguish it from COX4-1. The structure -function of COX4-2 orthologs in other vertebrates remains uncertain. Phylogenetic analyses suggest the two paralogs arose in basal vertebrates, but COX4-2 orthologs diverged faster than COX4-1 orthologs. COX4-1/4-2 protein levels in tilapia tracked mRNA levels across tissues, and did not change in hypoxia, arguing against a role for differential post-translational regulation of paralogs...
February 1, 2017: American Journal of Physiology. Regulatory, Integrative and Comparative Physiology
https://www.readbyqxmd.com/read/28129719/differences-in-reperfusion-induced-mitochondrial-oxidative-stress-and-cell-death-between-hippocampal-ca1-and-ca3-subfields-is-due-to-the-mitochondrial-thioredoxin-system
#19
Bocheng Yin, German Barrionuevo, Ines Batinic-Haberle, Mats Sandberg, Stephen Weber
AIMS: The susceptibility of CA1 over CA3 to damage from cerebral ischemia may be related to the differences in reactive oxygen species (ROS) production/removal between the two hippocampal subfields. We aimed to measure CA1/CA3 differences in net ROS production in real time in the first thirty minutes of reperfusion in pyramidal cells. We aimed to determine the underlying cause of the differential vulnerability of CA1 and CA3. RESULTS: Real-time determinations of mitochondrial H2O2 and, independently, glutathione (GSH) redox status from roGFP-based probes in individual pyramidal cells in organotypic hippocampal cultures during oxygen-glucose deprivation (OGD)-reperfusion (RP) demonstrate a significantly more oxidizing environment during reperfusion in CA1 than CA3 mitochondria...
January 27, 2017: Antioxidants & Redox Signaling
https://www.readbyqxmd.com/read/28127559/variety-of-rnas-in-peripheral-blood-cells-plasma-and-plasma-fractions
#20
Anna V Savelyeva, Elena V Kuligina, Dmitry N Bariakin, Vadim V Kozlov, Elena I Ryabchikova, Vladimir A Richter, Dmitry V Semenov
Human peripheral blood contains RNA in cells and in extracellular membrane vesicles, microvesicles and exosomes, as well as in cell-free ribonucleoproteins. Circulating mRNAs and noncoding RNAs, being internalized, possess the ability to modulate vital processes in recipient cells. In this study, with SOLiD sequencing technology, we performed identification, classification, and quantification of RNAs from blood fractions: cells, plasma, plasma vesicles pelleted at 16,000g and 160,000g, and vesicle-depleted plasma supernatant of healthy donors and non-small cell lung cancer (NSCLC) patients...
2017: BioMed Research International
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