Cross-talk between calcium and reactive oxygen species originated from NADPH oxidase in abscisic acid-induced antioxidant defence in leaves of maize seedlings

2003 ◽  
Vol 26 (6) ◽  
pp. 929-939 ◽  
Author(s):  
M. JIANG ◽  
J. ZHANG
Keyword(s):  
Reactive Oxygen Species ◽  
Abscisic Acid ◽  
Nadph Oxidase ◽  
Cross Talk ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Maize Seedlings ◽  
Antioxidant Defence

scholarly journals Cross talk between increased intracellular zinc (Zn2+) and accumulation of reactive oxygen species in chemical ischemia

2017 ◽  
Vol 313 (4) ◽  
pp. C448-C459 ◽  
Author(s):  
Kira G. Slepchenko ◽  
Qiping Lu ◽  
Yang V. Li
Keyword(s):  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Cross Talk ◽  
Reactive Oxygen ◽  
Glucose Deprivation ◽  
Ros Generation ◽  
Oxygen Species ◽  
Mitochondrial Ros ◽  
Ros Accumulation ◽  
Ischemic Stress

Both zinc (Zn2+) and reactive oxygen species (ROS) have been shown to accumulate during hypoxic-ischemic stress and play important roles in pathological processes. To understand the cross talk between the two of them, here we studied Zn2+ and ROS accumulation by employing fluorescent probes in HeLa cells to further the understanding of the cause and effect relationship of these two important cellular signaling systems during chemical-ischemia, stimulated by oxygen and glucose deprivation (OGD). We observed two Zn2+ rises that were divided into four phases in the course of 30 min of OGD. The first Zn2+ rise was a transient, which was followed by a latent phase during which Zn2+ levels recovered; however, levels remained above a basal level in most cells. The final phase was the second Zn2+ rise, which reached a sustained plateau called Zn2+ overload. Zn2+ rises were not observed when Zn2+ was removed by TPEN (a Zn2+ chelator) or thapsigargin (depleting Zn2+ from intracellular stores) treatment, indicating that Zn2+ was from intracellular storage. Damaging mitochondria with FCCP significantly reduced the second Zn2+ rise, indicating that the mitochondrial Zn2+ accumulation contributes to Zn2+ overload. We also detected two OGD-induced ROS rises. Two Zn2+ rises preceded two ROS rises. Removal of Zn2+ reduced or delayed OGD- and FCCP-induced ROS generation, indicating that Zn2+ contributes to mitochondrial ROS generation. There was a Zn2+-induced increase in the functional component of NADPH oxidase, p47phox, thus suggesting that NADPH oxidase may mediate Zn2+-induced ROS accumulation. We suggest a new mechanism of cross talk between Zn2+ and mitochondrial ROS through positive feedback processes that eventually causes excessive free Zn2+ and ROS accumulations during the course of ischemic stress.

scholarly journals ASCORBATE PEROXIDASE6 Protects Arabidopsis Desiccating and Germinating Seeds from Stress and Mediates Cross Talk between Reactive Oxygen Species, Abscisic Acid, and Auxin

2014 ◽  
Vol 166 (1) ◽  
pp. 370-383 ◽  
Author(s):  
Changming Chen ◽  
Ilya Letnik ◽  
Yael Hacham ◽  
Petre Dobrev ◽  
Bat-Hen Ben-Daniel ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Abscisic Acid ◽  
Cross Talk ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Germinating Seeds

21 Cross talk between reactive oxygen species producing mitochondria and NADPH oxidase

Mitochondrion ◽  
2007 ◽  
Vol 7 (6) ◽  
pp. 410
Author(s):  
Mariola Kulawiec ◽  
Mohamed M. Desouki ◽  
Keshav K. Singh
Keyword(s):  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Cross Talk ◽  
Reactive Oxygen ◽  
Oxygen Species

Ligation of lymphocyte function-associated antigen-1 on monocytes decreases very late antigen-4-mediated adhesion through a reactive oxygen species-dependent pathway

Blood ◽  
2004 ◽  
Vol 104 (13) ◽  
pp. 4046-4053 ◽  
Author(s):  
Kuo-Pin Chuang ◽  
Ya-Fang Huang ◽  
Yi-Ling Hsu ◽  
Hsiao-Sheng Liu ◽  
Hong-Chen Chen ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Adhesion Molecule ◽  
Cross Talk ◽  
Reactive Oxygen ◽  
Cellular Adhesion ◽  
Lymphocyte Function ◽  
Oxygen Species ◽  
Late Antigen ◽  
Nadph Oxidase Activation

Abstract Monocyte-endothelial adhesion plays an important role in monocyte trafficking and hence is important for immune responses and pathogenesis of inflammatory diseases including atherosclerosis. The cross-talk between different integrins on monocytes may be crucial for a coordinated regulation of the cellular adhesion during the complex process of transendothelial migration. By using monoclonal antibodies and recombinant intercellular adhesion molecule 1 (ICAM-1) to engage lymphocyte function-associated antigen 1 (LFA-1) on monocytic cells, we found that the cellular adhesion to vascular cell adhesion molecule 1 (VCAM-1) mediated by very late antigen 4 (VLA-4) was suppressed after this treatment and the suppression depended on the presence of reactive oxygen species (ROSs). Inhibition of production of ROSs through the use of inhibitor of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, but not inhibitors of mitochondrial electron transport chain or xanthine oxidase, revealed that this suppression on VLA-4-mediated cellular binding was mediated by ROSs produced by phagocyte NADPH oxidase. Activation of phosphoinositol-3 kinase and Akt appears to mediate this NADPH oxidase activation through p47phox phosphorylation and Rac-1 activation. Our results provide a novel pathway in which ROSs play a critical role in integrin cross-talk in monocytes. This signaling pathway may be important for cellular transition from firm arrest to diapedesis during monocyte trafficking. (Blood. 2004;104:4046-4053)

scholarly journals Role of NADPH Oxidase-Mediated Reactive Oxygen Species in Podocyte Injury

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Shan Chen ◽  
Xian-Fang Meng ◽  
Chun Zhang
Keyword(s):  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Epithelial To Mesenchymal Transition ◽  
Kidney Diseases ◽  
Treatment Strategies ◽  
Reactive Oxygen ◽  
Glomerular Sclerosis ◽  
Oxygen Species ◽  
Podocyte Injury ◽  
Mesenchymal Transition

Proteinuria is an independent risk factor for end-stage renal disease (ESRD) (Shankland, 2006). Recent studies highlighted the mechanisms of podocyte injury and implications for potential treatment strategies in proteinuric kidney diseases (Zhang et al., 2012). Reactive oxygen species (ROS) are cellular signals which are closely associated with the development and progression of glomerular sclerosis. NADPH oxidase is a district enzymatic source of cellular ROS production and prominently expressed in podocytes (Zhang et al., 2010). In the last decade, it has become evident that NADPH oxidase-derived ROS overproduction is a key trigger of podocyte injury, such as renin-angiotensin-aldosterone system activation (Whaley-Connell et al., 2006), epithelial-to-mesenchymal transition (Zhang et al., 2011), and inflammatory priming (Abais et al., 2013). This review focuses on the mechanism of NADPH oxidase-mediated ROS in podocyte injury under different pathophysiological conditions. In addition, we also reviewed the therapeutic perspectives of NADPH oxidase in kidney diseases related to podocyte injury.

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