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Oxphos AND Resveratrol

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https://www.readbyqxmd.com/read/29146241/cardiac-progenitor-cells-activated-by-mitochondrial-delivery-of-resveratrol-enhance-the-survival-of-a-doxorubicin-induced-cardiomyopathy-mouse-model-via-the-mitochondrial-activation-of-a-damaged-myocardium
#1
Jiro Abe, Yuma Yamada, Takeda Atsuhito, Hideyoshi Harashima
It has been reported that transplanting native cells would lack efficiency without producing artificial cell-tissue, due to the exaggerated oxidative stress in doxorubicin-induced cardiomyopathy. We attempted to activate cardiac progenitor cells (CPCs) by delivering resveratrol to mitochondria using a mitochondrial drug delivery system (MITO-Porter system). We first evaluated the viability of H9c2 cells (a cardio myoblast cell line) after doxorubicin treatment, where H9c2 cells were co-cultured with or without the mitochondria activated CPCs (referred to herein as MITO cell)...
November 13, 2017: Journal of Controlled Release: Official Journal of the Controlled Release Society
https://www.readbyqxmd.com/read/28973657/in-vitro-characterization-of-mitochondrial-function-and-structure-in-rat-and-human-cells-with-a-deficiency-of-the-nadh-ubiquinone-oxidoreductase-ndufc2-subunit
#2
Salvatore Raffa, Cristina Scrofani, Sabatino Valente, Andrea Micaloni, Forte Maurizio, Franca Bianchi, Roberta Coluccia, Aron M Geurts, Sebastiano Sciarretta, Massimo Volpe, Maria Rosaria Torrisi, Speranza Rubattu
Ndufc2, a subunit of the NADH:ubiquinone oxidoreductase, plays a key role in the assembly and activity of complex I within the mitochondrial OXPHOS chain. Its deficiency has been shown to be involved in diabetes, cancer and stroke. To improve our knowledge on the mechanisms underlying the increased disease risk due to Ndufc2 reduction, we performed the present in vitro study aimed at the fine characterization of the derangements in mitochondrial structure and function consequent to Ndufc2 deficiency. We found that both fibroblasts obtained from skin of heterozygous Ndufc2 knock-out rat model showed marked mitochondrial dysfunction and PBMC obtained from subjects homozygous for the TT genotype of the rs11237379/NDUFC2 variant, previously shown to associate with reduced gene expression, demonstrated increased generation of reactive oxygen species and mitochondrial damage...
August 30, 2017: Human Molecular Genetics
https://www.readbyqxmd.com/read/28906460/a-critical-assessment-of-the-therapeutic-potential-of-resveratrol-supplements-for-treating-mitochondrial-disorders
#3
REVIEW
Boel De Paepe, Rudy Van Coster
In human cells, mitochondria provide the largest part of cellular energy in the form of adenosine triphosphate generated by the process of oxidative phosphorylation (OXPHOS). Impaired OXPHOS activity leads to a heterogeneous group of inherited diseases for which therapeutic options today remain very limited. Potential innovative strategies aim to ameliorate mitochondrial function by increasing the total mitochondrial load of tissues and/or to scavenge the excess of reactive oxygen species generated by OXPHOS malfunctioning...
September 14, 2017: Nutrients
https://www.readbyqxmd.com/read/28817667/glycoprotein-ib-activation-by-thrombin-stimulates-the-energy-metabolism-in-human-platelets
#4
Norma Corona de la Peña, Manuel Gutiérrez-Aguilar, Ileana Hernández-Reséndiz, Álvaro Marín-Hernández, Sara Rodríguez-Enríquez
Thrombin-induced platelet activation requires substantial amounts of ATP. However, the specific contribution of each ATP-generating pathway i.e., oxidative phosphorylation (OxPhos) versus glycolysis and the biochemical mechanisms involved in the thrombin-induced activation of energy metabolism remain unclear. Here we report an integral analysis on the role of both energy pathways in human platelets activated by several agonists, and the signal transducing mechanisms associated with such activation. We found that thrombin, Trap-6, arachidonic acid, collagen, A23187, epinephrine and ADP significantly increased glycolytic flux (3-38 times vs...
2017: PloS One
https://www.readbyqxmd.com/read/28025489/the-effects-of-ascorbate-n-acetylcysteine-and-resveratrol-on-fibroblasts-from-patients-with-mitochondrial-disorders
#5
Liza Douiev, Devorah Soiferman, Corinne Alban, Ann Saada
Reactive oxygen species (ROS) are assumed to be implicated in the pathogenesis of inborn mitochondrial diseases affecting oxidative phosphorylation (OXPHOS). In the current study, we characterized the effects of three small molecules with antioxidant properties (N-acetylcysteine, ascorbate, and resveratrol) on ROS production and several OXPHOS parameters (growth in glucose free medium, ATP production, mitochondrial content and membrane potential (MMP)), in primary fibroblasts derived from seven patients with different molecularly defined and undefined mitochondrial diseases...
December 22, 2016: Journal of Clinical Medicine
https://www.readbyqxmd.com/read/26369791/transcriptome-analysis-of-complex-i-deficient-patients-reveals-distinct-expression-programs-for-subunits-and-assembly-factors-of-the-oxidative-phosphorylation-system
#6
Robin van der Lee, Radek Szklarczyk, Jan Smeitink, Hubert J M Smeets, Martijn A Huynen, Rutger Vogel
BACKGROUND: Transcriptional control of mitochondrial metabolism is essential for cellular function. A better understanding of this process will aid the elucidation of mitochondrial disorders, in particular of the many genetically unsolved cases of oxidative phosphorylation (OXPHOS) deficiency. Yet, to date only few studies have investigated nuclear gene regulation in the context of OXPHOS deficiency. In this study we performed RNA sequencing of two control and two complex I-deficient patient cell lines cultured in the presence of compounds that perturb mitochondrial metabolism: chloramphenicol, AICAR, or resveratrol...
2015: BMC Genomics
https://www.readbyqxmd.com/read/24606795/mitochondrial-biogenesis-pharmacological-approaches
#7
EDITORIAL
Teresa Valero
Organelle biogenesis is concomitant to organelle inheritance during cell division. It is necessary that organelles double their size and divide to give rise to two identical daughter cells. Mitochondrial biogenesis occurs by growth and division of pre-existing organelles and is temporally coordinated with cell cycle events [1]. However, mitochondrial biogenesis is not only produced in association with cell division. It can be produced in response to an oxidative stimulus, to an increase in the energy requirements of the cells, to exercise training, to electrical stimulation, to hormones, during development, in certain mitochondrial diseases, etc...
2014: Current Pharmaceutical Design
https://www.readbyqxmd.com/read/24334768/defining-the-action-spectrum-of-potential-pgc-1%C3%AE-activators-on-a-mitochondrial-and-cellular-level-in-vivo
#8
Annette Hofer, Natalie Noe, Christin Tischner, Nikolay Kladt, Veronika Lellek, Astrid Schauß, Tina Wenz
Previous studies have demonstrated a therapeutic benefit of pharmaceutical PGC-1α activation in cellular and murine model of disorders linked to mitochondrial dysfunction. While in some cases, this effect seems to be clearly associated with boosting of mitochondrial function, additional alterations as well as tissue- and cell-type-specific effects might play an important role. We initiated a comprehensive analysis of the effects of potential PGC-1α-activating drugs and pharmaceutically targeted the PPAR (bezafibrate, rosiglitazone), AMPK (AICAR, metformin) and Sirt1 (resveratrol) pathways in HeLa cells, neuronal cells and PGC-1α-deficient MEFs to get insight into cell type specificity and PGC-1α dependence of their working action...
May 1, 2014: Human Molecular Genetics
https://www.readbyqxmd.com/read/24102298/turn-up-the-power-pharmacological-activation-of-mitochondrial-biogenesis-in-mouse-models
#9
REVIEW
J C Komen, D R Thorburn
The oxidative phosphorylation (OXPHOS) system in mitochondria is responsible for the generation of the majority of cellular energy in the form of ATP. Patients with genetic OXPHOS disorders form the largest group of inborn errors of metabolism. Unfortunately, there is still a lack of efficient therapies for these disorders other than management of symptoms. Developing therapies has been complicated because, although the total group of OXPHOS patients is relatively large, there is enormous clinical and genetic heterogeneity within this patient population...
April 2014: British Journal of Pharmacology
https://www.readbyqxmd.com/read/19712747/bioenergetics-of-lung-tumors-alteration-of-mitochondrial-biogenesis-and-respiratory-capacity
#10
COMPARATIVE STUDY
N Bellance, G Benard, F Furt, H Begueret, K Smolková, E Passerieux, J P Delage, J M Baste, P Moreau, R Rossignol
Little is known on the metabolic profile of lung tumors and the reminiscence of embryonic features. Herein, we determined the bioenergetic profiles of human fibroblasts taken from lung epidermoid carcinoma (HLF-a) and fetal lung (MRC5). We also analysed human lung tumors and their surrounding healthy tissue from four patients with adenocarcinoma. On these different models, we measured functional parameters (cell growth rates in oxidative and glycolytic media, respiration, ATP synthesis and PDH activity) as well as compositional features (expression level of various energy proteins and upstream transcription factors)...
December 2009: International Journal of Biochemistry & Cell Biology
https://www.readbyqxmd.com/read/16968735/cytotoxicity-of-a-mutant-huntingtin-fragment-in-yeast-involves-early-alterations-in-mitochondrial-oxphos-complexes-ii-and-iii
#11
Asun Solans, Andrea Zambrano, Mayra Rodríguez, Antoni Barrientos
Mitochondrial dysfunction may play an important role in the pathogenic mechanism of Huntington's disease (HD). However, the exact mechanism by which mutated huntingtin could cause bioenergetic dysfunction is still unknown. We have constructed a stable inducible yeast model of HD by expressing a human huntingtin fragment containing a mutant polyglutamine tract of 103Q fused to green fluorescent protein (GFP), and a control expressing a wild-type 25Q domain fused to GFP in a wild-type strain. We showed that in yeast cells expressing 103Q, cell respiration was progressively reduced after 4-6 h of induction with galactose, down to 50% of the control after 10 h of induction...
October 15, 2006: Human Molecular Genetics
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