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Source: Redox Biology
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Total 62 results found since Jan 2013.
Brd4 inhibition attenuates unilateral ureteral obstruction-induced fibrosis by blocking TGF- β-mediated Nox4 expression
In conclusion, these results indicated that the inhibition of Brd4 might protect against renal fibrosis by blocking the TGF-β-Nox4-ROS-fibrosis axis, suggesting that Brd4 could be a promising therapeutic target. Graphical abstract
Source: Redox Biology - December 30, 2016 Category: Biology Source Type: research
Autophagy regulates turnover of lipid droplets via ROS-dependent Rab25 activation in hepatic stellate cell
In this study, we sought to investigate the role of autophagy in the process of LD disappearance, and to further examine the underlying mechanisms in this molecular context. We found that LD disappearance during HSC activation was associated with a coordinate increase in autophagy. Inhibition or depletion of autophagy by Atg5 siRNA impaired LD disappearance of quiescent HSCs, and also restored lipocyte phenotype of activated HSCs. In contrast, induction of autophagy by Atg5 plasmid accelerated LD loss of quiescent HSCs. Importantly, our study also identified a crucial role for reactive oxygen species (ROS) in the facilitat...
Source: Redox Biology - December 21, 2016 Category: Biology Source Type: research
The Mitochondria-targeted Antioxidant MitoQ Ameliorated Tubular Injury Mediated by Mitophagy in Diabetic Kidney Disease via Nrf2/PINK1
Publication date: Available online 21 December 2016 Source:Redox Biology Author(s): Li Xiao, Xiaoxuan Xu, Fan Zhang, Ming Wang, Yan Xu, Dan Tang, Jiahui Wang, Yan Qin, Yu Liu, Chengyuan Tang, Liyu He, Anna Greka, Zhiguang Zhou, Fuyou Liu, Dong Zeng, Lin Sun Mitochondria play a crucial role in tubular injury in diabetic kidney disease (DKD). MitoQ is a mitochondria-targeted antioxidant that exerts protective effects in diabetic mice, but the mechanism underlying these effects is not clear. We demonstrated that mitochondrial abnormalities, such as defective mitophagy, mitochondrial reactive oxygen species (ROS) overexpressi...
Source: Redox Biology - December 20, 2016 Category: Biology Source Type: research
Parkin Deficiency Exacerbate Ethanol-Induced Dopaminergic Neurodegeneration by P38 Pathway dependent inhibition of autophagy and mitochondrial function
Publication date: Available online 8 December 2016 Source:Redox Biology Author(s): Chul Ju Hwang, Young Eun Kim, Dong Ju Son, Mi Hee Park, Dong-Young Choi, Pil-Hoon Park, Sang-Bae Han, Ki-Wan Oh, Jin Tae Hong Parkinson's disease (PD) is a neurodegenerative disease characterized by selective degeneration of dopaminergic neurons in the substantia nigra. Parkin (which encoded by Park2), an E3 ubiquitin ligase, is the most frequently mutated gene that has casually been linked to autosomal recessive early onset familial PD. We tested the effect of Park2 on ethanol-induced dopaminergic neurodegeneration in Park2 knockout (KO) t...
Source: Redox Biology - December 7, 2016 Category: Biology Source Type: research
Advanced Oxidation Protein Products Sensitized the Transient Receptor Potential Vanilloid 1 via NADPH Oxidase 1 and 4 to Cause Mechanical Hyperalgesia
In conclusion, AOPPs increased significantly in CFA-induced hyperalgesia rats and they activated Nox1/Nox4-ROS to sensitize TRPV1-dependent Ca2+ influx and CGRP release which led to inducing mechanical hyperalgesia. Graphical abstract
Source: Redox Biology - September 17, 2016 Category: Biology Source Type: research
Connexin43 Hemichannels Contributes to the Disassembly of Cell Junctions through Modulation of Intracellular Oxidative Status
Publication date: Available online 21 August 2016 Source:Redox Biology Author(s): Yuan Chi, Xiling Zhang, Zhen zhang, Takahiko Mitsui, Manabu Kamiyama, Masayuki Takeda, Jian Yao Connexin (Cx) hemichannels regulate many cellular processes with little information available regarding their mechanisms. Given that many pathological factors that activate hemichannels also disrupts the integrity of cellular junctions, we speculated a potential participation of hemichannels in the regulation of cell junctions. Here we tested this hypothesis. Exposure of renal tubular epithelial cells to Ca2+-free medium led to disassembly of tigh...
Source: Redox Biology - August 20, 2016 Category: Biology Source Type: research
Hydrogen sulfide metabolism regulates endothelial solute barrier function
Publication date: Available online 11 August 2016 Source:Redox Biology Author(s): Shuai Yuan, Sibile Pardue, Xinggui Shen, J. Steven Alexander, A. Wayne Orr, Christopher G. Kevil Hydrogen sulfide (H2S) is an important gaseous signaling molecule in the cardiovascular system. In addition to free H2S, H2S can be oxidized to polysulfide which can be biologically active. Since the impact of H2S on endothelial solute barrier function is not known, we sought to determine whether H2S and its various metabolites affect endothelial permeability. In vitro permeability was evaluated using albumin flux and transendothelial electrical ...
Source: Redox Biology - August 10, 2016 Category: Biology Source Type: research
Glutathione S-transferase pi modulates NF-κB activation and pro-inflammatory responses in lung epithelial cells
The objective of the present study was to determine whether GSTP regulates NF-κB signaling, S-glutathionylation of IKK, and subsequent pro-inflammatory signaling. We demonstrated that, in unstimulated cells, GSTP associated with the inhibitor of NF-κB, IκBα. However, exposure to LPS resulted in a rapid loss of association between IκBα and GSTP, and instead led to a protracted association between IKKβ and GSTP. LPS exposure also led to increases in the S-glutathionylation of IKKβ. SiRNA-mediated knockdown of GSTP decreased IKKβ-SSG, and enhanced NF-κB nuclear translocation, transcriptional activity, and pro-inflam...
Source: Redox Biology - April 5, 2016 Category: Biology Source Type: research
PARP-1 inhibition influences the oxidative stress response of the human lens
Publication date: Available online 7 March 2016 Source:Redox Biology Author(s): Andrew J.O. Smith, Simon S.R. Ball, Richard P. Bowater, I. Michael Wormstone Poly(ADP-ribose) polymerase-1 (PARP-1) is best characterised for its involvement in DNA repair. PARP-1 activity is also linked to cell fate, confounding its roles in maintaining genome integrity. The current study assessed the functional roles of PARP-1 within human lens cells in response to oxidative stress. The human lens epithelial cell line FHL124 and whole human lens cultures were used as experimental systems. Hydrogen peroxide (H2O2) was employed to induce ...
Source: Redox Biology - March 8, 2016 Category: Biology Source Type: research
Role of Heme Oxygenase-1 in Low Dose Radioadaptive Response
In this study, we focused on the possible role of heme oxygenase 1 (HO-1) in RAR. Consistent with previous studies, priming dose of X-ray radiation (1-10cGy) induced significant RAR in normal human skin fibroblasts (AG 1522 cells). Transcription and translation of HO-1 was up-regulated more than two fold by a priming dose of radiation (5cGy). Zinc protoporphyrin Ⅸ, a specific competitive inhibitor of HO-1, efficiently inhibited RAR whereas hemin, an inducer of HO-1, could mimic priming dose of X-rays to induce RAR. Knocking down of HO-1 by transfection of HO-1 siRNA significantly attenuated RAR. Furthermore, the expressi...
Source: Redox Biology - March 5, 2016 Category: Biology Source Type: research
The novel triterpenoid RTA 408 protects human retinal pigment epithelial cells against H2O2-induced cell injury via NF-E2-related factor 2 (Nrf2) activation
In conclusion, our data suggest that RTA 408 protect primary human RPE cells from oxidative stress-induced damage by activating Nrf2 and its downstream genes.
Source: Redox Biology - December 20, 2015 Category: Biology Source Type: research
Redox balance influences differentiation status of neuroblastoma in the presence of all-trans retinoic acid
In this study, the expression of a common neuronal differentiation marker [neurofilament M (NF-M)] in human SK-N-SH neuroblastoma cells treated with 10μM all-trans retinoic acid (ATRA) showed significantly increased expression in accordance with reduced cell number. This was accompanied by an increase in MitoSOX and DCFH2 oxidation that could be indicative of increased steady-state levels of reactive oxygen species (ROS) such as O2 •− and H2O2, which correlated with increased levels of MnSOD activity and immuno-reactive protein. Furthermore PEG-catalase inhibited the DCFH2 oxidation signal to a greater extent in the A...
Source: Redox Biology - December 8, 2015 Category: Biology Source Type: research
Expression of xCT and activity of system xc− are regulated by NRF2 in human breast cancer cells in response to oxidative stress
Publication date: Available online 18 March 2015 Source:Redox Biology Author(s): Eric Habib , Katja Linher-Melville , Han-Xin Lin , Gurmit Singh Cancer cells adapt to high levels of oxidative stress in order to survive and proliferate by activating key transcription factors. One such master regulator, the redox sensitive transcription factor NF E2 Related Factor 2 (NRF2), controls the expression of cellular defense genes including those encoding intracellular redox-balancing proteins involved in glutathione (GSH) synthesis. Under basal conditions, Kelch-like ECH-associated protein 1 (KEAP1) targets NRF2 for ubiquitinatio...
Source: Redox Biology - March 18, 2015 Category: Biology Source Type: research
Induction of heme oxygenase-1 contributes to survival of Mycobacterium abscessus in human macrophages-like THP-1 cells
Publication date: Available online 20 January 2015 Source:Redox Biology Author(s): Maher Y. Abdalla , Iman M. Ahmad , Barbara Switzer , Bradley E. Britigan Mycobacterium abscessus (M.abs) is a rapidly growing mycobacterial species that infects macrophages, and is an important pathogen in patients with cystic fibrosis. We studied the early stages of M.abs infection of macrophages, with emphasis on the role of heme-oxygenase-1 (HO-1) in this infection. THP-1 cells were activated using TPA into macrophage-like cells and infected with M.abs for different time points. M.abs infection robustly induced HO-1 expression in the TH...
Source: Redox Biology - January 23, 2015 Category: Biology Source Type: research
Epalrestat increases glutathione, thioredoxin, and heme oxygenase-1 by stimulating Nrf2 pathway in endothelial cells
Publication date: Available online 10 December 2014 Source:Redox Biology Author(s): Kaori Yama , Keisuke Sato , Natsuki Abe , Yu Murao , Ryosuke Tatsunami , Yoshiko Tampo Epalrestat (EPS) is the only aldose reductase inhibitor that is currently available for the treatment of diabetic neuropathy. Recently, we found that EPS at near-plasma concentration increases the intracellular levels of glutathione (GSH) in rat Schwann cells. GSH plays a crucial role in protecting endothelial cells from oxidative stress, thereby preventing vascular diseases. Here we show that EPS increases GSH levels in not only Schwann cells but also ...
Source: Redox Biology - December 14, 2014 Category: Biology Source Type: research
