The Role of Reactive Nitrogen Species (RNS) in the Activation of Nuclear Factor Kappa B (NFkB) and Its Implications for Biological Systems: The Question of Balance

Ljubuncic, Predrag; Bar-Shai, Marina; Reznick, Abraham Z.

doi:10.1007/978-1-4020-8399-0_4

Cited by 4 publications

(4 citation statements)

References 250 publications

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“…Redox PTMs can also regulate the activity of several transcription factors (Brigelius-Flohé and Flohé, 2011 ). For instance, oxidation, S-nitrosation or nitration of p53, activating protein 1, myocyte enhancer factor 2 or nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) modulate the DNA binding and activity of these important transcription factors (Abate et al, 1990 ; Schreck et al, 1991 ; Rainwater et al, 1995 ; Klatt et al, 1999 ; Kabe et al, 2005 ; Yakovlev et al, 2007 ; Jung et al, 2008 ; Ljubuncic et al, 2008 ; Okamoto et al, 2014 ; Caviedes et al, 2020 ). Redox PTMs can also affect the activity of transcription factors through indirect mechanisms.…”

Section: Role Of Redox Ptms Of Protein Thiols In Cell Physiology and mentioning

confidence: 99%

Redox Post-translational Modifications of Protein Thiols in Brain Aging and Neurodegenerative Conditions—Focus on S-Nitrosation

Finelli

2020

Front. Aging Neurosci.

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Reactive oxygen species and reactive nitrogen species (RONS) are by-products of aerobic metabolism. RONS trigger a signaling cascade that can be transduced through oxidation-reduction (redox)-based post-translational modifications (redox PTMs) of protein thiols. This redox signaling is essential for normal cellular physiology and coordinately regulates the function of redox-sensitive proteins. It plays a particularly important role in the brain, which is a major producer of RONS. Aberrant redox PTMs of protein thiols can impair protein function and are associated with several diseases. This mini review article aims to evaluate the role of redox PTMs of protein thiols, in particular S-nitrosation, in brain aging, and in neurodegenerative diseases. It also discusses the potential of using redox-based therapeutic approaches for neurodegenerative conditions.

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Section: Role Of Redox Ptms Of Protein Thiols In Cell Physiology and mentioning

confidence: 99%

Redox Post-translational Modifications of Protein Thiols in Brain Aging and Neurodegenerative Conditions—Focus on S-Nitrosation

Finelli

2020

Front. Aging Neurosci.

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“…Even though ROS/RNS are known to be deleterious for cells, they also represent important and necessary signaling molecules [ 89 , 90 ]. Therefore, the balance between oxidant/antioxidant molecules must be finely tuned to avoid uncontrolled signaling mechanisms as demonstrated, for instance, by nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), which is up- or down-regulated by ROS/RNS in concentration- and cell-dependent manners [ 91 , 92 ].…”

Section: Extraosseous Calcificationmentioning

confidence: 99%

“…Mitochondrial ROS and RNS have been shown to activate NF-κB and NF-κB-dependent osteo-inductive signaling pathways ( Figure 2 B) [ 91 , 93 ]. NF-κB is located in the cytoplasm in a latent form that binds to several inhibitory proteins (IκBs) and can be activated by classical or alternative pathways [ 92 ].…”

Section: Extraosseous Calcificationmentioning

confidence: 99%

“…Oxidative stress up-regulates the expression of Runx2 through the activation of the phosphatidylinositol 3-kinase/protein kinase-B/Runx2 signaling pathway (PI3K/AKT/Runx2) or the p38 MAP kinase signaling pathway [ 91 , 99 ] leading to osteogenic trans-differentiation and promoting calcification [ 100 , 101 ] ( Figure 2 B). Moreover, ROS/RNS up-regulate bone morphogenetic protein-2 and -4 (BMP2 and BMP4) expression [ 102 , 103 , 104 ], which, through SMADs, act on several transcription factors such as Runx2, muscle segment homeobox 2 (Mxs2), and osterix, essential for pro-osteoblastic differentiation ( Figure 2 B) [ 105 ].…”

Section: Extraosseous Calcificationmentioning

confidence: 99%

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Apoptosis in the Extraosseous Calcification Process

Boraldi

Lofaro

Quaglino

2021

Cells

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Extraosseous calcification is a pathologic mineralization process occurring in soft connective tissues (e.g., skin, vessels, tendons, and cartilage). It can take place on a genetic basis or as a consequence of acquired chronic diseases. In this last case, the etiology is multifactorial, including both extra- and intracellular mechanisms, such as the formation of membrane vesicles (e.g., matrix vesicles and apoptotic bodies), mitochondrial alterations, and oxidative stress. This review is an overview of extraosseous calcification mechanisms focusing on the relationships between apoptosis and mineralization in cartilage and vascular tissues, as these are the two tissues mostly affected by a number of age-related diseases having a progressively increased impact in Western Countries.

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Different susceptibility of prefrontal cortex and hippocampus to oxidative stress following chronic social isolation stress

et al. 2014

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Chronic oxidative stress plays an important role in depression. The aim of present study was to examine the stress-induced changes in serum corticosterone (CORT) levels, cytosolic protein carbonyl groups, malondialdehyde (MDA), reduced glutathione (GSH), nitric oxide (NO) and total superoxide dismutase (SOD) activity in the prefrontal cortex versus hippocampus of male Wistar rats exposed to acute (2 h of immobilization or cold), chronic (21d of social isolation) stress, and their combination (chronic + acute stress). The subcellular distribution of nuclear factor-κB (NF-κB) and cytosolic cyclooxygenase 2 (COX-2) protein expressions were also examined. Depressive- and anxiety-like behaviors were assessed via the forced swim, sucrose preference, and marble burying tests in chronically isolated rats. Although both acute stressors resulted in elevated CORT, increased MDA in the prefrontal cortex and NF-κB activation accompanied by increased NO in the hippocampus were detected only following acute cold stress. Chronic isolation resulted in no change in CORT levels, but disabled appropriate response to novel acute stress and led to depressive- and anxiety-like behaviors. Increased oxidative/nitrosative stress markers, likely by NF-κB nuclear translocation and concomitant COX-2 upregulation, associated with decreased SOD activity and GSH levels, suggested the existence of oxidative stress in the prefrontal cortex. In contrast, hippocampus was less susceptible to oxidative damage showing only increase in protein carbonyl groups and depleted GSH. Taken together, the prefrontal cortex seems to be more sensitive to oxidative stress than the hippocampus following chronic isolation stress, which may be relevant for further research related to stress-induced depressive-like behavior.

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The Role of Reactive Nitrogen Species (RNS) in the Activation of Nuclear Factor Kappa B (NFkB) and Its Implications for Biological Systems: The Question of Balance

Cited by 4 publications

References 250 publications

Redox Post-translational Modifications of Protein Thiols in Brain Aging and Neurodegenerative Conditions—Focus on S-Nitrosation

Redox Post-translational Modifications of Protein Thiols in Brain Aging and Neurodegenerative Conditions—Focus on S-Nitrosation

Apoptosis in the Extraosseous Calcification Process

Different susceptibility of prefrontal cortex and hippocampus to oxidative stress following chronic social isolation stress

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