Human 8-oxoguanine DNA glycosylase increases resistance to hyperoxic cytotoxicity in lung epithelial cells and involvement with altered MAPK activity

Kannan, Shibichakravarthy; Pang, Huanhuan; Foster, Donald C.; Rao, Zihe; Wu, Min

doi:10.1038/sj.cdd.4401736

Cited by 49 publications

(46 citation statements)

References 54 publications

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“…For example, a decrease in hOGG1 confers cellular hypersensitivity to H 2 O 2 (30), and hOGG1-deficient human leukemia cells (KG-1) could be forced to undergo apoptosis by 8-hydroxyguanosine (31). On the other hand, the expression of hOGG1 suppresses the oxidative stress -derived DNA damages, followed by the enhanced cell survival (32)(33)(34). However, the exact mechanism by which oxidative stress -mediated DNA damage causes cell death is unclear.…”

Section: Discussionmentioning

confidence: 99%

Human 8-Oxoguanine DNA Glycosylase Suppresses the Oxidative Stress–Induced Apoptosis through a p53-Mediated Signaling Pathway in Human Fibroblasts

Youn¹,

Song

Kim³

et al. 2007

Molecular Cancer Research

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Human 8-oxoguanine DNA glycosylase (hOGG1) is the main defense enzyme against mutagenic effects of cellular 7,8-dihydro-8-oxoguanine. In this study, we investigated the biological role of hOGG1 in DNA damage -related apoptosis induced by hydrogen peroxide (H 2 O 2 ) -derived oxidative stress. The down-regulated expression of hOGG1 by its small interfering RNA prominently triggers the H 2 O 2 -induced apoptosis in human fibroblasts GM00637 and human lung carcinoma H1299 cells via the p53-mediated apoptotic pathway. However, the apoptotic responses were specifically inhibited by hOGG1 overexpression.

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Section: Discussionmentioning

confidence: 99%

Human 8-Oxoguanine DNA Glycosylase Suppresses the Oxidative Stress–Induced Apoptosis through a p53-Mediated Signaling Pathway in Human Fibroblasts

Youn¹,

Song

Kim³

et al. 2007

Molecular Cancer Research

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“…Recently, Hyun et al (2000) demonstrated that OGG1-deficient human leukemia cells might be required to undergo apoptosis by 8-OhdG. Conversely, expression of OGG1 suppressed oxidative stress derived DNA damage and enhanced cell survival (Kannan et al 2006).…”

Section: Discussionmentioning

confidence: 99%

Triphlorethol-A Improves the Non-Homologous End Joining and Base-Excision Repair Capacity Impaired by Formaldehyde

Zhang

Kang

Piao

et al. 2011

Journal of Toxicology and Environmental Health, Part A

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“…Cells were incubated with primary Abs at a 1:500 dilution in blocking buffer for 1 h and washed three times with wash buffer. After incubation with appropriate fluorophore-conjugated secondary Abs, the coverslips were mounted on slides with VECTASHIELD mounting medium (36). DAPI (SigmaAldrich) was used to stain the nucleus.…”

Section: Confocal Microscopy and Indirect Immunofluorescencementioning

confidence: 99%

Elevated Inflammatory Response in Caveolin-1-deficient Mice with Pseudomonas aeruginosa Infection Is Mediated by STAT3 Protein and Nuclear Factor κB (NF-κB)

Yuan

Huang

Fox

et al. 2011

Journal of Biological Chemistry

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Caveolin-1 (Cav-1), an important composition protein within the flask-shaped membrane invaginations termed caveolae, may play a role in host defense against infections. However, the phenotype in Pseudomonas aeruginosa-infected cav1 knock-out (KO) mice is still unresolved, and the mechanism involved is almost entirely unknown. Using a respiratory infection model, we confirmed a crucial role played by Cav-1 in host defense against this pathogen because Cav-1 KO mice showed increased mortality, severe lung injury, and systemic dissemination as compared with wild-type (WT) littermates. In addition, cav1 KO mice exhibited elevated inflammatory cytokines (IL-6, TNF-␣, and IL-12a), decreased phagocytic ability of macrophages, and increased superoxide release in the lung, liver, and kidney. We further studied relevant cellular signaling processes and found that STAT3 and NF-B are markedly activated. Our data revealed that the Cav-1/STAT3/NF-B axis is responsible for a dysregulated cytokine response, which contributes to increased mortality and disease progression. Moreover, downregulating Cav-1 in cell culture with a dominant negative strategy demonstrated that STAT3 activation was essential for the translocation of NF-B into the nucleus, confirming the observations from cav1 KO mice. Collectively, our studies indicate that Cav-1 is critical for inflammatory responses regulating the STAT3/NF-B pathway and thereby impacting P. aeruginosa infection.Pseudomonas aeruginosa accounts for 25% of Gram-negative bacteria isolated from hospitals and is associated with high morbidity and mortality (1). P. aeruginosa frequently infects immunocompromised individuals, such as those affected by ventilator-associated infection, severe burns, and cancer (2). More than 80% of cystic fibrosis patients suffer severe P. aeruginosa infection (3). This bacterium becomes increasingly resistant to various antibiotics. Further understanding the mechanism of the host-pathogen interaction may result in effective approaches to preventing this infection. Thus, P. aeruginosa has been a focus of airway infectious diseases (1, 4 -6).Recent studies suggest that P. aeruginosa also invades the lung epithelial cells through lipid raft-mediated endocytosis (7-9), which is a possible reason why this bacterium develops such formidable resistance to antibiotics (10). The invasion process of P. aeruginosa may involve certain lipid raft-associated proteins, including the caveolin family of proteins (9). Using caveolin-1 (cav1) 3 KO mice, two recent studies investigated the role of Cav-1 during P. aeruginosa infection (11, 12); however, their observations were very different. Thus, the role of Cav-1 in this infection needs to be clearly characterized.Caveolins are a family of integral membrane proteins involved in caveola formation and receptor-dependent endocytosis (13-15). Cav-1 and -2 are co-expressed in various cells, such as endothelial cells, airway epithelial cells, and type I pneumocytes. Cav-1 is the major component of caveolae, flaskshaped plasma membran...

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Human 8-oxoguanine DNA glycosylase increases resistance to hyperoxic cytotoxicity in lung epithelial cells and involvement with altered MAPK activity

Cited by 49 publications

References 54 publications

Human 8-Oxoguanine DNA Glycosylase Suppresses the Oxidative Stress–Induced Apoptosis through a p53-Mediated Signaling Pathway in Human Fibroblasts

Human 8-Oxoguanine DNA Glycosylase Suppresses the Oxidative Stress–Induced Apoptosis through a p53-Mediated Signaling Pathway in Human Fibroblasts

Triphlorethol-A Improves the Non-Homologous End Joining and Base-Excision Repair Capacity Impaired by Formaldehyde

Elevated Inflammatory Response in Caveolin-1-deficient Mice with Pseudomonas aeruginosa Infection Is Mediated by STAT3 Protein and Nuclear Factor κB (NF-κB)

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