Helicobacter pylori and H2O2 increase AP endonuclease-1/redox factor-1 expression in human gastric epithelial cells

Ding, Song; O'Hara, Ann M; Denning, Timothy L.; Dirden-Kramer, Bernadette; Mifflin, Randy C.; Reyes, Victor E.; Ryan, Kevin; Elliott, Susan N.; Izumi, Tohru; Boldogh, István; Mitra, Sankar; Ernst, Peter B.; Crowe, Sheila E.

doi:10.1053/j.gastro.2004.06.017

Cited by 81 publications

(74 citation statements)

References 53 publications

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“…Studies have shown that infection with H. pylori generates ROS (29), resulting in the accumulation of ROS within the gastric mucosa (18) including the epithelial cells (30), which, in turn, leads to oxidative DNA damage (31) in infected patients. Previously, we reported that treatment with hydrogen peroxide as well as infection with H. pylori, but not Campylobacter jejuni, enhanced APE-1/Ref-1 expression in human gastric epithelial cells (32). Moreover, altered levels or cellular location of APE-1/Ref-1 have been found in some cancers, including ovarian and prostate (33,34), while an APE-1/Ref-1-like gene was recently shown to be up-regulated in gastric cancer (35).…”

Section: Interleukin-8 Induction By Helicobacter Pylori In Gastric Epmentioning

confidence: 85%

“…H. pylori infection status was determined in separate samples obtained for diagnostic purposes using histochemistry with immunostaining for H. pylori according to standard Department of Pathology (University of Virginia) diagnostic methods. Study biopsy samples were snap frozen and sections (8 m) were prepared and micro dissected as described previously (32). RNA was extracted from the captured cells using the Absolutely RNA nanoprep kit (Stratagene) and cDNA and no-RT controls were prepared.…”

Section: Isolation Of Human Gastric Epithelial Cells By Laser Capturementioning

confidence: 99%

“…Total cellular lysates were also analyzed by Western blotting to check the extent of silencing on the APE-1/Ref-1 level itself. After treating the cells with 300:1 H. pylori for 1 h (for NF-B) or 2 h (for AP-1), nuclear and total cell lysates were prepared using methods as described earlier (32). Protein concentrations were measured using a BCA protein assay reagent kit (Pierce).…”

Section: Assessment Of the Effect Of Ape-1/ref-1 Silencing On H Pylomentioning

confidence: 99%

“…Sitedirected mutations of the IL-8 AP-1 or NF-B binding sites in the context of the Ϫ162/ϩ44 hIL-8 promoter were introduced by the PCR overlap extension mutagenesis technique as described previously (45). The APE-1/Ref-1 expression vector pFLAG-APE-1 cDNA3.1 was prepared as described (32).…”

Section: Plasmidsmentioning

confidence: 99%

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Interleukin-8 Induction by Helicobacter pylori in Gastric Epithelial Cells is Dependent on Apurinic/Apyrimidinic Endonuclease-1/Redox Factor-1

O'Hara

Bhattacharyya

Mifflin³

et al. 2006

The Journal of Immunology

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Helicobacter pylori infection causes inflammation and increases the expression of IL-8 in human gastric epithelial cells. H. pylori activates NF-κB and AP-1, essential transcriptional factors in H. pylori-induced IL-8 gene transcription. Although colonization creates a local oxidative stress, the molecular basis for the transition from infection to the expression of redox-sensitive cytokine genes is unknown. We recently reported that the expression of apurinic/apyrimidinic endonuclease-1/redox factor-1 (APE-1/Ref-1), which repairs oxidative DNA damage and reductively activates transcription factors including AP-1 and NF-κB, is increased in human gastric epithelia during H. pylori infection. In this study, we examine whether APE-1/Ref-1 functions in the modulation of IL-8 gene expression in H. pylori-infected human gastric epithelial cells. Small interfering RNA-mediated silencing of APE-1/Ref-1 inhibited basal and H. pylori-induced AP-1 and NF-κB DNA-binding activity without affecting the nuclear translocation of these transcription factors and also reduced H. pylori-induced IL-8 mRNA and protein. In contrast, overexpression of APE-1/Ref-1 enhanced basal and H. pylori-induced IL-8 gene transcription, and the relative involvement of AP-1 in inducible IL-8 promoter activity was greater in APE-1/Ref-1 overexpressing cells than in cells with basal levels of APE-1/Ref-1. APE-1/Ref-1 inhibition also reduced other H. pylori-induced chemokine expression. By implicating APE-1/Ref-1 as an important regulator of gastric epithelial responses to H. pylori infection, these data elucidate a novel mechanism controlling transcription and gene expression in bacterial pathogenesis.

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Section: Interleukin-8 Induction By Helicobacter Pylori In Gastric Epmentioning

confidence: 85%

Section: Isolation Of Human Gastric Epithelial Cells By Laser Capturementioning

confidence: 99%

Section: Assessment Of the Effect Of Ape-1/ref-1 Silencing On H Pylomentioning

confidence: 99%

Section: Plasmidsmentioning

confidence: 99%

See 2 more Smart Citations

Interleukin-8 Induction by Helicobacter pylori in Gastric Epithelial Cells is Dependent on Apurinic/Apyrimidinic Endonuclease-1/Redox Factor-1

O'Hara

Bhattacharyya

Mifflin³

et al. 2006

The Journal of Immunology

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“…IL-8 also enhances neutrophil migration into the gastric epithelial layer and their subsequent activation (65,145), thereby further contributing to inflammation. We have reported that the expression of APE1/Ref1, which reductively activates transcription factors, is induced in H. pylori-infected human gastric epithelia (82). We have also shown that APE1/Ref1 expressed in gastric epithelial cells enhances transcriptional activity of AP1 and NF-B and induces H. pylori-mediated IL-8 expression (209).…”

Section: Peptic Ulcer Disease and Gastritismentioning

confidence: 94%

Oxidative Stress: An Essential Factor in the Pathogenesis of Gastrointestinal Mucosal Diseases

Bhattacharyya

Chattopadhyay

Mitra

et al. 2014

Physiological Reviews

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1,685

1,258

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Reactive oxygen species (ROS) are generated as by-products of normal cellular metabolic activities. Superoxide dismutase, glutathione peroxidase, and catalase are the enzymes involved in protecting cells from the damaging effects of ROS. ROS are produced in response to ultraviolet radiation, cigarette smoking, alcohol, nonsteroidal anti-inflammatory drugs, ischemia-reperfusion injury, chronic infections, and inflammatory disorders. Disruption of normal cellular homeostasis by redox signaling may result in cardiovascular, neurodegenerative diseases and cancer. ROS are produced within the gastrointestinal (GI) tract, but their roles in pathophysiology and disease pathogenesis have not been well studied. Despite the protective barrier provided by the mucosa, ingested materials and microbial pathogens can induce oxidative injury and GI inflammatory responses involving the epithelium and immune/inflammatory cells. The pathogenesis of various GI diseases including peptic ulcers, gastrointestinal cancers, and inflammatory bowel disease is in part due to oxidative stress. Unraveling the signaling events initiated at the cellular level by oxidative free radicals as well as the physiological responses to such stress is important to better understand disease pathogenesis and to develop new therapies to manage a variety of conditions for which current therapies are not always sufficient.

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Helicobacter pylori genotype and polymorphisms in DNA repair enzymes: Where do they correlate in gastric cancer?

Silva-Fernandes

Silva

Agnez-Lima

et al. 2012

Journal of Surgical Oncology

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Helicobacter pylori and H2O2 increase AP endonuclease-1/redox factor-1 expression in human gastric epithelial cells

Cited by 81 publications

References 53 publications

Interleukin-8 Induction by Helicobacter pylori in Gastric Epithelial Cells is Dependent on Apurinic/Apyrimidinic Endonuclease-1/Redox Factor-1

Interleukin-8 Induction by Helicobacter pylori in Gastric Epithelial Cells is Dependent on Apurinic/Apyrimidinic Endonuclease-1/Redox Factor-1

Oxidative Stress: An Essential Factor in the Pathogenesis of Gastrointestinal Mucosal Diseases

Helicobacter pylori genotype and polymorphisms in DNA repair enzymes: Where do they correlate in gastric cancer?

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