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Redox Biology

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https://www.readbyqxmd.com/read/29660505/gcn2-deficiency-ameliorates-doxorubicin-induced-cardiotoxicity-by-decreasing-cardiomyocyte-apoptosis-and-myocardial-oxidative-stress
#1
Yue Wang, Tong Lei, Juntao Yuan, Yongguang Wu, Xiyue Shen, Junling Gao, Wei Feng, Zhongbing Lu
The clinical use of doxorubicin for cancer therapy is limited by its cardiotoxicity, which involves cardiomyocyte apoptosis and oxidative stress. Previously, we showed that general control nonderepressible 2 (GCN2), an eukaryotic initiation factor 2α (eIF2α) kinase, impairs the ventricular adaptation to chronic pressure overload by affecting cardiomyocyte apoptosis. However, the impact of GCN2 on Dox-induced cardiotoxicity has not been investigated. In the present study, we treated wild type (WT) and Gcn2-/- mice with four intraperitoneal injections (5 mg/kg/week) to induce cardiomyopathy...
April 7, 2018: Redox Biology
https://www.readbyqxmd.com/read/29660503/high-circulatory-leptin-mediated-nox-2-peroxynitrite-mir21-axis-activate-mesangial-cells-and-promotes-renal-inflammatory-pathology-in-nonalcoholic-fatty-liver-disease
#2
Firas Alhasson, Ratanesh Kumar Seth, Sutapa Sarkar, Diana A Kimono, Muayad S Albadrani, Diptadip Dattaroy, Varun Chandrashekaran, Geoffrey I Scott, Samir Raychoudhury, Mitzi Nagarkatti, Prakash Nagarkatti, Anna Mae Diehl, Saurabh Chatterjee
High circulatory insulin and leptin followed by underlying inflammation are often ascribed to the ectopic manifestations in non-alcoholic fatty liver disease (NAFLD) but the exact molecular pathways remain unclear. We have shown previously that CYP2E1-mediated oxidative stress and circulating leptin in NAFLD is associated with renal disease severity. Extending the studies, we hypothesized that high circulatory leptin in NAFLD causes renal mesangial cell activation and tubular inflammation via a NOX2 dependent pathway that upregulates proinflammatory miR21...
April 7, 2018: Redox Biology
https://www.readbyqxmd.com/read/29660504/idh2-deficiency-accelerates-skin-pigmentation-in-mice-via-enhancing-melanogenesis
#3
Jung Hyun Park, Hyeong Jun Ku, Jin Hyup Lee, Jeen-Woo Park
Melanogenesis is a complex biosynthetic pathway regulated by multiple agents, which are involved in the production, transport, and release of melanin. Melanin has diverse roles, including determination of visible skin color and photoprotection. Studies indicate that melanin synthesis is tightly linked to the interaction between melanocytes and keratinocytes. α-melanocyte-stimulating hormone (α-MSH) is known as a trigger that enhances melanin biosynthesis in melanocytes through paracrine effects. Accumulated reactive oxygen species (ROS) in skin affects both keratinocytes and melanocytes by causing DNA damage, which eventually leads to the stimulation of α-MSH production...
April 6, 2018: Redox Biology
https://www.readbyqxmd.com/read/29649787/defective-protein-repair-under-methionine-sulfoxide-a-deletion-drives-autophagy-and-are-dependent-gene-transcription
#4
Steven M Pennington, Paula R Klutho, Litao Xie, Kim Broadhurst, Olha M Koval, Michael L McCormick, Douglas R Spitz, Isabella M Grumbach
OBJECTIVE: Reduction of oxidized methionines is emerging as a major protein repair pathway. The lack of methionine sulfoxide reductase A (MsrA) exacerbates cardiovascular disease phenotypes driven by increased oxidative stress. However, the role of MsrA on maintaining cellular homeostasis in the absence of excessive oxidative stress is less well understood. METHODS AND RESULTS: Constitutive genetic deletion of MsrA increased formation of p62-containing protein aggregates, activated autophagy, and decreased a marker of apoptosis in vascular smooth muscle cells (VSMC)...
April 3, 2018: Redox Biology
https://www.readbyqxmd.com/read/29653411/autophagy-inhibition-attenuates-hyperoxaluria-induced-renal-tubular-oxidative-injury-and-calcium-oxalate-crystal-depositions-in-the-rat-kidney
#5
Xiaolu Duan, Zhenzhen Kong, Xin Mai, Yu Lan, Yang Liu, Zhou Yang, Zhijian Zhao, Tuo Deng, Tao Zeng, Chao Cai, Shujue Li, Wen Zhong, Wenqi Wu, Guohua Zeng
Hyperoxaluria-induced oxidative injury of renal tubular epithelial cell is a casual and essential factor in kidney calcium oxalate (CaOx) stone formation. Autophagy has been shown to be critical for the regulation of oxidative stress-induced renal tubular injury; however, little is known about its role in kidney CaOx stone formation. In the present study, we found that the autophagy antagonist chloroquine could significantly attenuate oxalate-induced autophagy activation, oxidative injury and mitochondrial damage of renal tubular cells in vitro and in vivo, as well as hyperoxaluria-induced CaOx crystals depositions in rat kidney, whereas the autophagy agonist rapamycin exerted contrasting effects...
April 2, 2018: Redox Biology
https://www.readbyqxmd.com/read/29631100/sa-inhibits-complex-iii-activity-to-generate-reactive-oxygen-species-and-thereby-induces-ga-overproduction-in-ganoderma-lucidum
#6
Rui Liu, Pengfei Cao, Ang Ren, Shengli Wang, Tao Yang, Ting Zhu, Liang Shi, Jing Zhu, Ai-Liang Jiang, Ming-Wen Zhao
Ganoderma lucidum has high commercial value because it produces many active compounds, such as ganoderic acids (GAs). Salicylic acid (SA) was previously reported to induce the biosynthesis of GA in G. lucidum. In this study, we found that SA induces GA biosynthesis by increasing ROS production, and further research found that NADPH oxidase-silenced strains exhibited a partial reduction in the response to SA, resulting in the induction of increased ROS production. Furthermore, the localization of ROS shows that mitochondria are sources of ROS production in response to SA treatment...
March 31, 2018: Redox Biology
https://www.readbyqxmd.com/read/29597144/vitamin-k-redox-modulation-prevention-of-mitochondrial-dysfunction-and-anticancer-effect
#7
Donika Ivanova, Zhivko Zhelev, Plamen Getsov, Biliana Nikolova, Ichio Aoki, Tatsuya Higashi, Rumiana Bakalova
This review is directed to the redox-modulating properties and anticancer effect of vitamin K. The concept is focused on two aspects: (i) redox-cycle of vitamin K and its effect on the calcium homeostasis, "oncogenic" and "onco-suppressive" reactive oxygen species and the specific induction of oxidative stress in cancer; (ii) vitamin K plus C as a powerful redox-system, which forms a bypass between mitochondrial complexes II and III and thus prevents mitochondrial dysfunction, restores oxidative phosphorylation and aerobic glycolysis, modulates the redox-state of endogenous redox-pairs, eliminates the hypoxic environment of cancer cells and induces cell death...
March 20, 2018: Redox Biology
https://www.readbyqxmd.com/read/29587245/mitochondrial-ros-cause-motor-deficits-induced-by-synaptic-inactivity-implications-for-synapse-pruning
#8
Eva Sidlauskaite, Jack W Gibson, Ian L Megson, Philip D Whitfield, Artak Tovmasyan, Ines Batinic-Haberle, Michael P Murphy, Peter R Moult, James N Cobley
Developmental synapse pruning refines burgeoning connectomes. The basic mechanisms of mitochondrial reactive oxygen species (ROS) production suggest they select inactive synapses for pruning: whether they do so is unknown. To begin to unravel whether mitochondrial ROS regulate pruning, we made the local consequences of neuromuscular junction (NMJ) pruning detectable as motor deficits by using disparate exogenous and endogenous models to induce synaptic inactivity en masse in developing Xenopus laevis tadpoles...
March 20, 2018: Redox Biology
https://www.readbyqxmd.com/read/29587244/epigenetic-regulation-of-vascular-nadph-oxidase-expression-and-reactive-oxygen-species-production-by-histone-deacetylase-dependent-mechanisms-in-experimental-diabetes
#9
Simona-Adriana Manea, Mihaela-Loredana Antonescu, Ioana Madalina Fenyo, Monica Raicu, Maya Simionescu, Adrian Manea
Reactive oxygen species (ROS) generated by up-regulated NADPH oxidase (Nox) contribute to structural-functional alterations of the vascular wall in diabetes. Epigenetic mechanisms, such as histone acetylation, emerged as important regulators of gene expression in cardiovascular disorders. Since their role in diabetes is still elusive we hypothesized that histone deacetylase (HDAC)-dependent mechanisms could mediate vascular Nox overexpression in diabetic conditions. Non-diabetic and streptozotocin-induced diabetic C57BL/6J mice were randomized to receive vehicle or suberoylanilide hydroxamic acid (SAHA), a pan-HDAC inhibitor...
March 17, 2018: Redox Biology
https://www.readbyqxmd.com/read/29579719/copper-accumulation-in-senescent-cells-interplay-between-copper-transporters-and-impaired-autophagy
#10
Shashank Masaldan, Sharnel A S Clatworthy, Cristina Gamell, Zoe M Smith, Paul S Francis, Delphine Denoyer, Peter M Meggyesy, Sharon La Fontaine, Michael A Cater
Cellular senescence is characterized by irreversible growth arrest incurred through either replicative exhaustion or by pro-oncogenic cellular stressors (radioactivity, oxidative stress, oncogenic activation). The enrichment of senescent cells in tissues with age has been associated with tissue dyshomeostasis and age-related pathologies including cancers, neurodegenerative disorders (e.g. Alzheimer's, Parkinson's, etc.) and metabolic disorders (e.g. diabetes). We identified copper accumulation as being a universal feature of senescent cells [mouse embryonic fibroblasts (MEF), human prostate epithelial cells and human diploid fibroblasts] in vitro...
March 17, 2018: Redox Biology
https://www.readbyqxmd.com/read/29573704/the-uremic-toxin-hippurate-promotes-endothelial-dysfunction-via-the-activation-of-drp1-mediated-mitochondrial-fission
#11
Mengjie Huang, Ribao Wei, Yang Wang, Tingyu Su, Ping Li, Xiangmei Chen
The accumulation of uremic toxins in chronic kidney disease (CKD) induces inflammation, oxidative stress and endothelial dysfunction, which is a key step in atherosclerosis. Accumulating evidence indicates increased mitochondrial fission is a contributing mechanism for impaired endothelial function. Hippurate, a uremic toxin, has been reported to be involved in cardiovascular diseases. Here, we assessed the endothelial toxicity of hippurate and the contribution of altered mitochondrial dynamics to hippurate-induced endothelial dysfunction...
March 16, 2018: Redox Biology
https://www.readbyqxmd.com/read/29571125/nadph-oxidases-in-traumatic-brain-injury-promising-therapeutic-targets
#12
Merry W Ma, Jing Wang, Krishnan M Dhandapani, Ruimin Wang, Darrell W Brann
Traumatic brain injury (TBI) is a major cause of death and disability worldwide. Despite intense investigation, no neuroprotective agents for TBI have yet translated to the clinic. Recent efforts have focused on identifying potential therapeutic targets that underlie the secondary TBI pathology that evolves minutes to years following the initial injury. Oxidative stress is a key player in this complex cascade of secondary injury mechanisms and prominently contributes to neurodegeneration and neuroinflammation...
March 15, 2018: Redox Biology
https://www.readbyqxmd.com/read/29573705/peroxidasin-mediated-crosslinking-of-collagen-iv-is-independent-of-nadph-oxidases
#13
Gábor Sirokmány, Hajnal A Kovács, Enikő Lázár, Krisztina Kónya, Ágnes Donkó, Balázs Enyedi, Helmut Grasberger, Miklós Geiszt
Collagen IV is a major component of the basement membrane in epithelial tissues. The NC1 domains of collagen IV protomers are covalently linked together through sulfilimine bonds, the formation of which is catalyzed by peroxidasin. Although hydrogen peroxide is essential for this reaction, the exact source of the oxidant remains elusive. Members of the NOX/DUOX NADPH oxidase family are specifically devoted to the production of superoxide and hydrogen peroxide. Our aim in this study was to find out if NADPH oxidases contribute in vivo to the formation of collagen IV sulfilimine crosslinks...
March 14, 2018: Redox Biology
https://www.readbyqxmd.com/read/29573703/n-acetyl-cysteine-reverts-the-proinflammatory-state-induced-by-cigarette-smoke-extract-in-lung-calu-3-cells
#14
Ángel G Valdivieso, Andrea V Dugour, Verónica Sotomayor, Mariángeles Clauzure, Juan M Figueroa, Tomás A Santa-Coloma
Chronic obstructive pulmonary disease (COPD) and cystic fibrosis (CF) are lethal pulmonary diseases. Cigarette consumption is the main cause for development of COPD, while CF is produced by mutations in the CFTR gene. Although these diseases have a different etiology, both share a CFTR activity impairment and proinflammatory state even under sterile conditions. The aim of this work was to study the extent of the protective effect of the antioxidant N-acetylcysteine (NAC) over the proinflammatory state (IL-6 and IL-8), oxidative stress (reactive oxygen species, ROS), and CFTR levels, caused by Cigarette Smoke Extract (CSE) in Calu-3 airway epithelial cells...
March 14, 2018: Redox Biology
https://www.readbyqxmd.com/read/29548725/corrigendum-to-a-review-of-the-basics-of-mitochondrial-bioenergetics-metabolism-and-related-signaling-pathways-in-cancer-cells-therapeutic-targeting-of-tumor-mitochondria-with-lipophilic-cationic-compounds-redox-14c-2017-316-327
#15
Balaraman Kalyanaraman, Gang Cheng, Micael Hardy, Olivier Ouari, Marcos Lopez, Joy Joseph, Jacek Zielonka, Michael B Dwinell
No abstract text is available yet for this article.
March 13, 2018: Redox Biology
https://www.readbyqxmd.com/read/29627745/sorting-cells-alters-their-redox-state-and-cellular-metabolome
#16
Elizabeth M Llufrio, Lingjue Wang, Fuad J Naser, Gary J Patti
A growing appreciation of the metabolic artifacts of cell culture has generated heightened enthusiasm for performing metabolomics on populations of cells purified from tissues and biofluids. Fluorescence activated cell sorting, or FACS, is a widely used experimental approach to purify specific cell types from complex heterogeneous samples. Here we show that FACS introduces oxidative stress and alters the metabolic state of cells. Compared to unsorted controls, astrocytes subjected to FACS prior to metabolomic analysis showed altered ratios of GSSG to GSH, NADPH to NADP+ , and NAD+ to NADH...
March 9, 2018: Redox Biology
https://www.readbyqxmd.com/read/29549824/diverse-roles-of-mitochondria-in-ischemic-stroke
#17
REVIEW
Jenq-Lin Yang, Sujira Mukda, Shang-Der Chen
Stroke is the leading cause of adult disability and mortality in most developing and developed countries. The current best practices for patients with acute ischemic stroke include intravenous tissue plasminogen activator and endovascular thrombectomy for large-vessel occlusion to improve clinical outcomes. However, only a limited portion of patients receive thrombolytic therapy or endovascular treatment because the therapeutic time window after ischemic stroke is narrow. To address the current shortage of stroke management approaches, it is critical to identify new potential therapeutic targets...
March 9, 2018: Redox Biology
https://www.readbyqxmd.com/read/29549823/microrna-98-regulates-foam-cell-formation-and-lipid-accumulation-through-repression-of-lox-1
#18
Yao Dai, Xiaoqin Wu, Dongsheng Dai, Jun Li, Jawahar L Mehta
OBJECTIVE: Several miR/s that regulate gene/s relevant in atherogenesis are being described. We identified a miR (miR-98) that targets LOX-1, a receptor for ox-LDL, and speculated that it might be relevant in atherogenesis. APPROACH AND RESULTS: MicroRNA-98 was predicted by bioinformatics tools. The effects of miR-98 (by use of mimics and inhibitors) on LOX-1 expression and foam cell formation in mouse peritoneal macrophages were assessed. ApoE-/- mice fed by high fat diet were administered with mmu-agomiR-98 and mmu-antagomiR-98, and expression of LOX-1 and foam cell formation in aorta were quantified...
March 8, 2018: Redox Biology
https://www.readbyqxmd.com/read/29547847/lipid-peroxidation-regulates-podocyte-migration-and-cytoskeletal-structure-through-redox-sensitive-rhoa-signaling
#19
Claudia Kruger, Susan J Burke, J Jason Collier, Trang-Tiffany Nguyen, J Michael Salbaum, Krisztian Stadler
Early podocyte loss is characteristic of chronic kidney diseases (CKD) in obesity and diabetes. Since treatments for hyperglycemia and hypertension do not prevent podocyte loss, there must be additional factors causing podocyte depletion. The role of oxidative stress has been implicated in CKD but it is not known how exactly free radicals affect podocyte physiology. To assess this relationship, we investigated the effects of lipid radicals on podocytes, as lipid peroxidation is a major form of oxidative stress in diabetes...
March 6, 2018: Redox Biology
https://www.readbyqxmd.com/read/29524841/protective-effect-of-dioscin-against-doxorubicin-induced-cardiotoxicity-via-adjusting-microrna-140-5p-mediated-myocardial-oxidative-stress
#20
Lisha Zhao, Xufeng Tao, Yan Qi, Lina Xu, Lianhong Yin, Jinyong Peng
Clinical application of doxorubicin (DOX) is limited because of its cardiotoxicity. Thus, exploration of effective lead compounds against DOX-induced cardiotoxicity is necessary. The aim of the present study was to investigate the effects and possible mechanisms of dioscin against DOX-induced cardiotoxicity. The in vitro model of DOX- treated H9C2 cells and the in vivo models of DOX-treated rats and mice were used in this study. The results showed that discoin markedly increased H9C2 cell viability, decreased the levels of CK, LDH, and improved histopathological and electrocardio- gram changes in rats and mice to protect DOX-induced cardiotoxicity...
March 6, 2018: Redox Biology
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