Reactive Oxygen Species as Intracellular Messengers During Cell Growth and Differentiation

Sauer, Heinrich; Wartenberg, Maria; Hescheler, Juergen

doi:10.1159/000047804

Cited by 1,013 publications

(693 citation statements)

References 122 publications

(101 reference statements)

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“…The cellular ROS are primarily produced intracellularly by two metabolic sources: the mitochondrial electron-transport chain and oxygenmetabolizing enzymatic reactions in mitochondria, such as xanthine oxidases, the cytochrome P450 system and NADPH oxidases (Bredt et al, 1991;Sauer et al, 2001;Sarsour et al, 2009). ROS were traditionally thought of as toxic byproducts in cells, which damaged cellular macromolecules and led cells to apoptosis (Shackelford et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

Functional interaction of Ugene and EBV infection mediates tumorigenic effects

et al. 2011

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Epstein-Barr virus (EBV) infection is associated with many human neoplasms, in which EBV-derived latent membrane protein-1 (LMP1) appears to be critical, but its exact oncogenic mechanism remains to be defined. To this end, our initial microarray analyses identified a LMP1-inducible gene, Ugene, originally characterized as a binding partner for uracil DNA glycosylase 2, which is highly expressed in malignant colon cancer. In this report, it was found that Ugene, designated herein as LMP1-induced protein (LMPIP), was induced, in a time-dependent manner, in EBV-infected peripheral blood mononuclear cells and LMP1-transfected 293 cells. Functionally, when compared with mock-transfected cells, overexpression of LMPIP in nasopharyngeal carcinoma (NPC) cell lines resulted in a decrease in reactive oxygen species production and maintained mitochondria membrane potential (Dw) loss induced by H 2 O 2 . The NPC cells transfected with LMPIP also showed a decrease in G1 population and an increase in the cell population in sub-G1 and multiploid phase, concomitant with increased levels of cell cycle activators, including cyclin D1 and CDK4. In contrast, silencing of LMPIP expression in the NPC tumor cell lines with short hairpin RNA interference revealed significantly decreased cell population at G1/S phase, while the number of cells in multiploid phase increased. Significantly, NPC cells with LMPIP knock-down also showed a decrease in tumorigenic and transforming activity induced by ectopic LMP1 expression, as determined by analyses of soft agar foci and tumor size in nude mice. Further, elevated LMPIP expression was also noted in cytoplasm and nuclei in EBVinfected NPC tumor cell mass and non-EBV-infected tumor cell lines. These results suggested that LMPIP may have an important mediator role in EBV-mediated neoplasm and may serve as a new target for therapy of tumors induced by EBV infection.

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Section: Discussionmentioning

confidence: 99%

Functional interaction of Ugene and EBV infection mediates tumorigenic effects

et al. 2011

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“…In a redox balance, reactive species play an important role in the life cycle of cells (including development, physiology and migration) [13], the induction of cell signaling pathways [14], the activation of intra-and intercellular secondary messengers [15] and immune cell defense mechanisms during phagocytosis of pathogenic agents [16]. RNS are also involved in the regulation of blood pressure and vascular tone [12], the activation of NFκβ by TLR-4 receptors [17], the release of inammatory cytokines and the expression of adhesion molecules [18].…”

Section: Reactive Speciesmentioning

confidence: 99%

Sepsis, mitochondrial failure and multiple organ dysfunction

Dúran-Bedolla

Oca-Sandoval²,

Saldaña-Navor³

et al. 2014

CIM

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Purpose: e purpose of this review is to consider the state of oxidative stress, failure of the antioxidant systems and mitochondrial failure as the main physiopathological mechanisms leading to multiple organ dysfunction during sepsis.Principal ndings: Sepsis is a clinical syndrome caused by a severe infection that triggers an exaggerated in ammatory response. Involved in the pathogenesis of sepsis are the activation of in ammatory, immune, hormonal, metabolic and bioenergetic responses. One of the pivotal factors in these processes is the increase of reactive species accompanied by the failure of the antioxidant systems, leading to a state of irreversible oxidative stress and mitochondrial failure.In a physiological state, reactive species and antioxidant systems are in redox balance. e loss of this balance during both chronic and infectious diseases leads to a state of oxidative stress, which is considered to be the greatest promoter of a systemic in ammatory response.e loss of the redox balance, together with a systemic in ammatory response during sepsis, can lead to progressive and irreversible mitochondrial failure, energy depletion, hypoxia, septic shock, severe sepsis, multiple organ dysfunction and death of the patient. Conclusion:Knowledge of the molecular processes associated with the development of oxidative stress should facilitate the development of e ective therapies and better prognosis for patients with sepsis and organ dysfunction.

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“…17 It is well known that ROS are linked with cellular signaling as second messengers. 23,24 Thus, transient elevation of endogenously generated ROS and an appropriate amount of exogenously treated ROS are essential to mediating signal transduction. Together, these previous reports indicate that various oxidative stresses are responsible for cellular transcription factor activation.…”

Section: Inhibitory Effect Of Combined Rankl and Bso On Cell Growthmentioning

confidence: 99%

Regulation of osteoclast differentiation by the redox-dependent modulation of nuclear import of transcription factors

Kim

et al. 2005

Cell Death Differ

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This study sought to characterize the reduced glutathione (GSH)/oxidized GSSG ratio during osteoclast differentiation and determine whether changes in the intracellular redox status regulate its differentiation through a RANKL-dependent signaling pathway. A progressive decrease of the GSH/ GSSG ratio was observed during osteoclast differentiation, and the phenomenon was dependent on a decrease in total glutathione via downregulation of expression of the cglutamylcysteinyl synthetase modifier gene. Glutathione depletion by L-buthionine-(S,R)-sulfoximine (BSO) was found to inhibit osteoclastogenesis by blocking nuclear import of NF-jB and AP-1 in RANKL-propagated signaling and bone pit formation by increasing BSO concentrations in mature osteoclasts. Furthermore, intraperitoneal injection of BSO in mice resulted in an increase in bone density and a decrease of the number of osteoclasts in bone. Conversely, glutathione repletion with either N-acetylcysteine or GSH enhanced osteoclastogenesis. These findings indicate that redox status decreases during osteoclast differentiation and that this modification directly regulates RANKL-induced osteoclastogenesis.

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Reactive Oxygen Species as Intracellular Messengers During Cell Growth and Differentiation

Cited by 1,013 publications

References 122 publications

Functional interaction of Ugene and EBV infection mediates tumorigenic effects

Functional interaction of Ugene and EBV infection mediates tumorigenic effects

Sepsis, mitochondrial failure and multiple organ dysfunction

Regulation of osteoclast differentiation by the redox-dependent modulation of nuclear import of transcription factors

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