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PubMed Central (PMC3 - NLM DTD) (2,682,705 recursos)
Archive of life sciences journal literature at the U.S. National Institutes of Health (NIH), developed and managed by NIH's National Center for Biotechnology Information (NCBI) in the National Library of Medicine (NLM).

Antioxidants & Redox Signaling

Mostrando recursos 1 - 20 de 648

1. Secisbp2 Is Essential for Embryonic Development and Enhances Selenoprotein Expression - Seeher, Sandra; Atassi, Tarik; Mahdi, Yassin; Carlson, Bradley A.; Braun, Doreen; Wirth, Eva K.; Klein, Marc O.; Reix, Nathalie; Miniard, Angela C.; Schomburg, Lutz; Hatfield, Dolph L.; Driscoll, Donna M.; Schweizer, Ulrich
Aims: The selenocysteine insertion sequence (SECIS)-binding protein 2 (Secisbp2) binds to SECIS elements located in the 3′-untranslated region of eukaryotic selenoprotein mRNAs. Selenoproteins contain the rare amino acid selenocysteine (Sec). Mutations in SECISBP2 in humans lead to reduced selenoprotein expression thereby affecting thyroid hormone-dependent growth and differentiation processes. The most severe cases also display myopathy, hearing impairment, male infertility, increased photosensitivity, mental retardation, and ataxia. Mouse models are needed to understand selenoprotein-dependent processes underlying the patients' pleiotropic phenotypes. Results: Unlike tRNA[Ser]Sec-deficient embryos, homozygous Secisbp2-deleted embryos implant, but fail before gastrulation. Heterozygous inactivation of Secisbp2 reduced the amount of selenoprotein expressed,...

2. Nitroso-Redox Balance and Mitochondrial Homeostasis Are Regulated by STOX1, a Pre-Eclampsia-Associated Gene - Doridot, Ludivine; Châtre, Laurent; Ducat, Aurélien; Vilotte, Jean-Luc; Lombès, Anne; Méhats, Céline; Barbaux, Sandrine; Calicchio, Rosamaria; Ricchetti, Miria; Vaiman, Daniel
Aims: Storkhead box 1 (STOX1) is a winged-helix transcription factor that is implicated in the genetic forms of a high-prevalence human gestational disease, pre-eclampsia. STOX1 overexpression confers pre-eclampsia-like transcriptomic features to trophoblastic cell lines and pre-eclampsia symptoms to pregnant mice. The aim of this work was to evaluate the impact of STOX1 on free radical equilibrium and mitochondrial function, both in vitro and in vivo. Results: Transcriptome analysis of STOX1-transgenic versus nontransgenic placentas at 16.5 days of gestation revealed alterations of mitochondria-related pathways. Placentas overexpressing STOX1 displayed altered mitochondrial mass and were severely biased toward protein nitration, indicating nitroso-redox imbalance...

3. Redox Control of Inflammation in Macrophages - Brüne, Bernhard; Dehne, Nathalie; Grossmann, Nina; Jung, Michaela; Namgaladze, Dmitry; Schmid, Tobias; von Knethen, Andreas; Weigert, Andreas

4. Regulation of the Intrinsic Apoptosis Pathway by Reactive Oxygen Species - Wu, Chu-Chiao; Bratton, Shawn B.

5. Regulation of Cell Death by Transfer RNA - Hou, Ya-Ming; Yang, Xiaolu

6. Mitochondrial Phosphorylation in Apoptosis: Flipping the Death Switch - Niemi, Natalie M.; MacKeigan, Jeffrey P.

7. Oxidative Damage in Clinical Ischemia/Reperfusion Injury: A Reappraisal - de Vries, Dorottya K.; Kortekaas, Kirsten A.; Tsikas, Dimitrios; Wijermars, Leonie G.M.; van Noorden, Cornelis J.F.; Suchy, Maria-Theresia; Cobbaert, Christa M.; Klautz, Robert J.M.; Schaapherder, Alexander F.M.; Lindeman, Jan H.N.

8. New Insights into the Link Between DNA Damage and Apoptosis - De Zio, Daniela; Cianfanelli, Valentina; Cecconi, Francesco

9. Bioreducible Polycations as Shuttles for Therapeutic Nucleic Acid and Protein Transfection - Klein, Philipp M.; Wagner, Ernst

10. Glutaredoxin 2 Reduces Both Thioredoxin 2 and Thioredoxin 1 and Protects Cells from Apoptosis Induced by Auranofin and 4-Hydroxynonenal - Zhang, Huihui; Du, Yatao; Zhang, Xu; Lu, Jun; Holmgren, Arne

11. VEGFR2 Functions As an H2S-Targeting Receptor Protein Kinase with Its Novel Cys1045–Cys1024 Disulfide Bond Serving As a Specific Molecular Switch for Hydrogen Sulfide Actions in Vascular Endothelial Cells - Tao, Bei-Bei; Liu, Shu-Yuan; Zhang, Cai-Cai; Fu, Wei; Cai, Wen-Jie; Wang, Yi; Shen, Qing; Wang, Ming-Jie; Chen, Ying; Zhang, Li-Jia; Zhu, Yi-Zhun; Zhu, Yi-Chun

12. Prx I Suppresses K-ras-Driven Lung Tumorigenesis by Opposing Redox-Sensitive ERK/Cyclin D1 Pathway - Park, Young-Ho; Kim, Sun-Uk; Lee, Bo-Kyoung; Kim, Hyun-Sun; Song, In-Sung; Shin, Hye-Jun; Han, Ying-Hao; Chang, Kyu-Tae; Kim, Jin-Man; Lee, Dong-Seok; Kim, Yeul-Hong; Choi, Chang-Min; Kim, Bo-Yeon; Yu, Dae-Yeul

13. Bardoxolone Brings Nrf2-Based Therapies to Light - Zhang, Donna D.

14. Targeting Nitric Oxide Signaling with nNOS Inhibitors As a Novel Strategy for the Therapy and Prevention of Human Melanoma - Yang, Zhen; Misner, Bobbye; Ji, Haitao; Poulos, Thomas L.; Silverman, Richard B.; Meyskens, Frank L.; Yang, Sun

15. S-Nitrosoglutathione Reductase Deficiency-Induced S-Nitrosylation Results in Neuromuscular Dysfunction - Montagna, Costanza; Di Giacomo, Giuseppina; Rizza, Salvatore; Cardaci, Simone; Ferraro, Elisabetta; Grumati, Paolo; De Zio, Daniela; Maiani, Emiliano; Muscoli, Carolina; Lauro, Filomena; Ilari, Sara; Bernardini, Sergio; Cannata, Stefano; Gargioli, Cesare; Ciriolo, Maria R.; Cecconi, Francesco; Bonaldo, Paolo; Filomeni, Giuseppe
Aims: Nitric oxide (NO) production is implicated in muscle contraction, growth and atrophy, and in the onset of neuropathy. However, many aspects of the mechanism of action of NO are not yet clarified, mainly regarding its role in muscle wasting. Notably, whether NO production-associated neuromuscular atrophy depends on tyrosine nitration or S-nitrosothiols (SNOs) formation is still a matter of debate. Here, we aim at assessing this issue by characterizing the neuromuscular phenotype of S-nitrosoglutathione reductase-null (GSNOR-KO) mice that maintain the capability to produce NO, but are unable to reduce SNOs. Results: We demonstrate that, without any sign of protein nitration,...

16. NADPH Oxidase 1, a Novel Molecular Source of ROS in Hippocampal Neuronal Death in Vascular Dementia - Choi, Dong-Hee; Lee, Kyoung-Hee; Kim, Ji-Hye; Seo, Ju-Ha; Kim, Hahn Young; Shin, Chan Young; Han, Jung-Soo; Han, Seol-Heui; Kim, Yoon-Seong; Lee, Jongmin
Aims: Chronic cerebral hypoperfusion (CCH) is a common pathological factor that contributes to neurodegenerative diseases such as vascular dementia (VaD). Although oxidative stress has been strongly implicated in the pathogenesis of VaD, the molecular mechanism underlying the selective vulnerability of hippocampal neurons to oxidative damage remains unknown. We assessed whether the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (Nox) complex, a specialized superoxide generation system, plays a role in VaD by permanent ligation of bilateral common carotid arteries in rats. Results: Male Wistar rats (10 weeks of age) were subjected to bilateral occlusion of the common carotid arteries (two-vessel occlusion [2VO])....

17. Mitochondrial Morphology in Metabolic Diseases - Galloway, Chad A.; Yoon, Yisang
Significance: Mitochondria are the cellular energy-producing organelles and are at the crossroad of determining cell life and death. As such, the function of mitochondria has been intensely studied in metabolic disorders, including diabetes and associated maladies commonly grouped under all-inclusive pathological condition of metabolic syndrome. More recently, the altered metabolic profiles and function of mitochondria in these ailments have been correlated with their aberrant morphologies. This review describes an overview of mitochondrial fission and fusion machineries, and discusses implications of mitochondrial morphology and function in these metabolic maladies. Recent Advances: Mitochondria undergo frequent morphological changes, altering the mitochondrial network organization...

18. Why Mitochondria Must Fuse to Maintain Their Genome Integrity - Vidoni, Sara; Zanna, Claudia; Rugolo, Michela; Sarzi, Emmanuelle; Lenaers, Guy
Significance: The maintenance of mitochondrial genome integrity is a major challenge for cells to sustain energy production by respiration. Recent Advances: Recently, mitochondrial membrane dynamics emerged as a key process contributing to prevent mitochondrial DNA (mtDNA) alterations. Indeed, both fundamental and clinical data suggest that disruption of mitochondrial fusion, related to mutations in the OPA1, MFN2, PINK1, and PARK2 genes, leads to the accumulation of mutations in the mitochondrial genome. Critical Issues: We discuss here the possibility that mitochondrial fusion acts as a direct mechanism to prevent the generation of altered mtDNA and to eliminate mutated deleterious genomes either by...

19. Glucocorticoid Modulation of Mitochondrial Function in Hepatoma Cells Requires the Mitochondrial Fission Protein Drp1 - Hernández-Alvarez, María Isabel; Paz, José C.; Sebastián, David; Muñoz, Juan Pablo; Liesa, Marc; Segalés, Jessica; Palacín, Manuel; Zorzano, Antonio
Aims: Glucocorticoids, such as dexamethasone, enhance hepatic energy metabolism and gluconeogenesis partly through changes in mitochondrial function. Mitochondrial function is influenced by the balance between mitochondrial fusion and fission events. However, whether glucocorticoids modulate mitochondrial function through the regulation of mitochondrial dynamics is currently unknown. Results: Here, we report that the effects of dexamethasone on mitochondrial function and gluconeogenesis in hepatoma cells are dependent on the mitochondrial fission protein dynamin-related protein 1 (Drp1). Dexamethasone increased routine oxygen consumption, maximal respiratory capacity, superoxide anion, proton leak, and gluconeogenesis in hepatoma cells. Under these conditions, dexamethasone altered mitochondrial morphology, which was paralleled...

20. Does Scavenging of Mitochondrial Superoxide Attenuate Cancer Prosurvival Signaling Pathways? - Nazarewicz, Rafal R.; Dikalova, Anna; Bikineyeva, Alfiya; Ivanov, Sergey; Kirilyuk, Igor A.; Grigor'ev, Igor A.; Dikalov, Sergey I.
It has been previously suggested that overexpression of mitochondrial superoxide dismutase (SOD) attenuates cancer development; however, the exact mechanism remains unclear. In this work, we have studied the direct effect of the mitochondria-targeted superoxide scavenger, (2-(2,2,6,6-tetramethylpiperidin-1-oxyl-4-ylamino)-2-oxoethyl)triphenylphosphonium chloride (mitoTEMPO), on B16-F0 mouse melanoma cells and tumor growth in a nude mouse model of human melanoma. We show that scavenging of mitochondrial superoxide inhibited cell growth, reduced viability, and induced apoptosis in melanoma cells, but did not affect nonmalignant skin fibroblasts. Diminished mitochondrial superoxide inhibited redox-dependent Akt, restored activity of mitochondrial pyruvate dehydrogenase, and reduced HIF1-α and lactate dehydrogenase expression in cancer...

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