Regulation of Gene Expression by Reactive Oxygen

Dalton, Timothy P.; Shertzer, Howard G.; Puga, Alvaro

doi:10.1146/annurev.pharmtox.39.1.67

Cited by 1,009 publications

(593 citation statements)

References 259 publications

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“…The mutant mtDNA leads to mitochondria with impaired respiratory function [2]. In addition, ROS act as intracellular messenger and mediate lymphocyte activation [9] as well as apoptosis [5] by interacting with redox-sensitive transcription factors like NF B.…”

Section: Discussionmentioning

confidence: 99%

Age-related changes of apoptotic cell death in human lymphocytes

Schindowski

Leutner

Müller

et al. 2000

Neurobiology of Aging

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Apoptosis seems to be involved in irnmunosenescence associated with aging. Moreover, in lymphocytes (PBL) of patients with Akheimer's disease, an increased susceptibirity to the apoprotic pathway has been described possibly due to impaired protection o f oxidative stress. Accordingly. it seemed to be of particular interest to investigate the contribution of normal aging to the susceptibility from human lymphocytes 20 programmed cell death. We coiild show that PBL from elderly individuals (>60 years) accumuIate apoptosing cells to a significant higher extent in spontaneous and activation-induced cell death compared to younger controls (<35 years). Treatment with the oxidative Stressor 2-deoxy-D-ribose or with agonistic-CD95-antibody pronounced this effect even more implicating a higher sensitivity to reactive oxygen species and a higher functionril CD95 expression, respectively. In addition, expression of the activation markerc HLA-DR and CD95 was significantly increased in CD3 "-cells of aged subjects, while expression of CD25 did not seem to be affected by age.Expression of Bcl-2 was increased in aging and comlated with the number o f apoptotic cells.Kqwordv. &in& Apoptosis: 1,yrnphocytes; Oxidativc stress; dctivation markers; Bcl-2 Programmed cell death (PCD) or apoptosis is of particular interest in aging, as it is thought X o play an irnportant role in various age-related degenerative diseases. Apoptosis of white bIood cells could be one reason for the decrease of the total number of leukocytes and the decrease of the immune response with aging related Z o Cancer, infections, and autoirnmune disorders [3]. Several changes in lymphocytes have been observed related to aging: diminished synthesis of g r o~h and survive factos 146,511, impaired intracellular calcium regulation [18], different surface malecule expression 1431, and defects of signal transdi~ction [36]. Some of these pathological changes are additionally altered in patients witl~ Alzheimer's disease (AD), but are not present in vascular dementia [13][14][15]171. In order to differentiate common and divergent mechanisms of an enhanced susceptibility of lymphocytes to apoptosis in aging and sporadic AD, we investigated in detail the molecular basis of enhanced apoptosis in aged human lymphocytes. Oxidative Stress increases with aging and ltads to enhanced cellular damage (e.g. Iipidperoxidation, protein oxidation, DNA damage (for review see ref.[IO]). In addition, reactive axygen species (ROS) can trigger cells to undergo pragrammed cell death and can act as second rnessenger by influencing transcription factors like NF-KB and AP-I. Increased oxidative stress and decreased ability to cope with ROS could ampliQ apoptotic cell death in aging lymphocytes. BcI-2 acts in an antioxidative and antiapoptotic way and can interfcre with the apoptotic pathway 17,471.One oF the best known and characterized surface receptors related to PCD in lymphocytes is ApollFas (CD95), a rnernber of the himor necrosis factor (W) superfamily. Stimulation of this recep...

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Section: Discussionmentioning

confidence: 99%

Age-related changes of apoptotic cell death in human lymphocytes

Schindowski

Leutner

Müller

et al. 2000

Neurobiology of Aging

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“…By contrast, the redox balance can be shifted (positive) under conditions of oxidative stress over and above that which can be contained by endogenous protective mechanisms. Thiol oxidation ensues and a range of cellular processes are altered that may result in metabolic dysfunction, altered cellular fate, molecular damage and an amplified inflammatory response (for reviews see [37,38]). …”

Section: Redox Balancementioning

confidence: 99%

The pathogenesis of lung injury following pulmonary resection

Jordan¹,

Mitchell²,

Quinlan³

et al. 2000

Eur Respir J

235

115

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Postpneumonectomy pulmonary oedema (PPO) develops in~5% of patients undergoing pneumonectomy or lobectomy, and has a high associated mortality (>50%). In its extreme form, PPO follows a clinical and histopathological course indistinguishable from acute respiratory distress syndrome.Perioperative fluid overload, impaired lymphatic drainage following node dissection and trauma caused by surgical manipulation have been implicated in the pathogenesis of PPO. However, PPO more probably represents the pulmonary manifestation of a panendothelial injury consequent upon inflammatory processes induced by the surgical procedure, which involves collapse and re-expansion of the operative lung to permit hilar dissection and pulmonary resection.High inspired oxygen concentrations are required to overcome the effects of shunt. Animal studies have shown that pulmonary ischaemia/reperfusion can result in oedema formation, possibly due to the generation of pro-oxidant forces. Moreover, plasma taken from patients undergoing lobectomy or pneumonectomy (but not lesser resections) shows evidence of oxidative damage.Such evidence suggests either that the high inspired oxygen concentrations associated with one-lung ventilation, or ischaemia/reperfusion injury, may modulate postpneumonectomy pulmonary oedema. Mechanisms by which redox imbalance may result in tissue damage and postpneumonectomy pulmonary oedema are discussed. Eur Respir J 2000; 15: 790±799.

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“…Release of cytochrome c is an indicator of apoptosis; however, its extent depends on radiation exposure [30]. Exposure of cells to low dose radiation alters the intracellular redox balance by inducing oxidative stress and thereby depletion of intracellular antioxidants [14,31]. Therefore, extraneous supplementation of antioxidants serves as a useful buffer to protect cells from radiation (ROS)-induced injury [32].…”

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confidence: 99%

“…However, PEGcatalase, PEG-SOD, and vitamin C were inefficient in inhibiting the radiation-induced increase in CD20 expression. This may be due to their specificity for neutralizing a more limited range of free radicals than what is produced by radiation, which generates superoxide, H 2 O 2 , hydroxyl radical, nitric oxide, and peroxynitrite [15,28,31]. Strikingly, amifostine could completely inhibit the radiation-induced increase in CD20 levels.…”

mentioning

confidence: 99%

Regulation of CD20 expression by radiation-induced changes in intracellular redox status

Gupta

Crosby

Almasan

et al. 2008

Free Radical Biology and Medicine

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Increasing the levels of CD20 expression in cells that harbor low CD20 levels may enhance their responsiveness to CD20-specific antibody therapies. Here, we examined the regulation of CD20 expression after treatment with 0.5-2.0 Gy X-irradiation and hydrogen peroxide (H 2 O 2 ), in the presence or absence of known antioxidants, in the Burkitt lymphoma cell lines Daudi and Raji. Irradiation of cells enhanced cell-surface CD20 expression; the kinetics and extent of this change were cell-type specific and time-dependent. The kinetics of reactive oxygen species generation and changes in mitochondrial membrane potential after irradiation were also correlated with changes in CD20 expression. Raji and Daudi cells treated with H 2 O 2 showed a 2-to 2.5-fold increase in CD20 expression at 12 and 20 h, respectively. Buthionine sulfoximine, which depletes glutathione, also increased surface CD20, whereas antioxidants, such as PEG-catalase, PEG-SOD, vitamin C, and amifostine, decreased CD20 expression induced by radiation or H 2 O 2 . The antioxidant-mediated decrease in CD20 expression induced by radiation or H 2 O 2 suggests a mechanism involving redox regulation. These results demonstrate the critical role of radiationinduced oxidative stress in CD20 expression and may have implications for defining and improving the efficacy of CD20-targeted antibody therapy and radioimmunotherapy. Keywords CD20; Ionizing radiation; Reactive oxygen species; Antioxidants; Mitochondria; Mitochondrial membrane potential; Free radicals The CD20 transmembrane protein is exclusively expressed on B cells. It appears during the pre-B-cell stage, but is absent during the earlier or later stages of B cell differentiation, such as in antibody-secreting plasma cells [1,2]. CD20 has received extensive evaluation as an ideal target for immunotherapy and radioimmunotherapy, in part because of its ubiquitous expression on target cells, stable localization within the cell membrane, and absence from normal stem cells [3]. Rituximab, a chimeric monoclonal anti-CD20 antibody, has been used extensively in the treatment of low-grade B cell lymphomas, such as non-Hodgkin lymphoma (NHL) and other related pathologies. In clinical applications, the efficacy of Rituximab seems to fade after a period of months, leading to Rituximab resistance. The Recent studies have reported that bryostatin-1, interleukin-4, granulocyte-macrophage colony-stimulating factor, tumor necrosis factor-α, and interferon-α are all able to induce CD20 surface expression [8][9][10][11][12][13]. However, the mechanisms regulating the expression of CD20 remain poorly understood, even though these cytokines are well known to cause robust intracellular oxidative bursts [14,15]. Recently, it was shown that the bryostatin-1-induced increase of CD20 was regulated at the transcriptional level. The effect of bryostatin-1 on CD20 expression in NHL-derived cells was apparently mediated through the MAPK/ERK signal transduction pathway and involved protein kinase C [13]. Our group has previous...

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Regulation of Gene Expression by Reactive Oxygen

Cited by 1,009 publications

References 259 publications

Age-related changes of apoptotic cell death in human lymphocytes

Age-related changes of apoptotic cell death in human lymphocytes

The pathogenesis of lung injury following pulmonary resection

Regulation of CD20 expression by radiation-induced changes in intracellular redox status

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