A Novel Hypomorphic <i>Apex1</i> Mouse Model Implicates Apurinic/Apyrimidinic Endonuclease 1 in Oxidative DNA Damage Repair in Gastric Epithelial Cells

Ríos-Covián, David; Butcher, Lindsay D.; Ablack, Amber; Hartog, Gerco den; Mastsubara, Mason T; Ly, Hong; Oates, Andrew W; Xu, Guiyin; Fisch, Kathleen M.; Ahrens, Eric T.; Toden, Shusuke; Brown, Corrie C.; Kim, Kenneth; Le, Dzung; Eckmann, Lars; Dhar, Bithika; Izumi, Tohru; Ernst, Peter B.; Crowe, Sheila E.

doi:10.1089/ars.2021.0119

Cited by 3 publications

(3 citation statements)

References 59 publications

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“…Several lines of evidence point toward an association of APE‐1 and ROS‐mediated DNA damage upon H. pylori infection 157 . In vitro researches revealed that knockdown of APE‐1 in AGS cells following H. pylori stimulation results in substantially elevated levels of ROS and γH2AX, an indicator of DSBs, resulting in G2/M arrest and apoptosis 157,158 . In vivo study on transgenic mice with lower APE‐1 expression has also demonstrated hypersensitivity to oxidative stress and significantly higher DNA damage in H. pylori ‐infected mice than in control 158 .…”

Section: Host Damage and Gastric Cancermentioning

confidence: 99%

“…157 In vitro researches revealed that knockdown of APE-1 in AGS cells following H. pylori stimulation results in substantially elevated levels of ROS and γH2AX, an indicator of DSBs, resulting in G2/M arrest and apoptosis. 157,158 In vivo study on transgenic mice with lower APE-1 expression has also demonstrated hypersensitivity to oxidative stress and significantly higher DNA damage in H. pylori-infected mice than in control. 158 Moreover, a study has revealed that APE1 can dampen ROS generation during H. pylori infection by negative regulation of Rac1 and Nox1.…”

Section: Dna Damagementioning

confidence: 99%

“…157,158 In vivo study on transgenic mice with lower APE-1 expression has also demonstrated hypersensitivity to oxidative stress and significantly higher DNA damage in H. pylori-infected mice than in control. 158 Moreover, a study has revealed that APE1 can dampen ROS generation during H. pylori infection by negative regulation of Rac1 and Nox1. 39 Infection with cagA + H. pylori can trigger ROS production and DSBs in gastric epithelial cells.…”

Section: Dna Damagementioning

confidence: 99%

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Reactive oxygen species and gastric carcinogenesis: The complex interaction between Helicobacter pylori and host

Wu,

Chen,

Chen

et al. 2023

Helicobacter

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Helicobacter pylori (H. pylori) is a highly successful human pathogen that colonizes stomach in around 50% of the global population. The colonization of bacterium induces an inflammatory response and a substantial rise in the production of reactive oxygen species (ROS) and reactive nitrogen species (RNS), mostly derived from host neutrophils and gastric epithelial cells, which play a crucial role in combating bacterial infections. However, H. pylori has developed various strategies to quench the deleterious effects of ROS, including the production of antioxidant enzymes, antioxidant proteins as well as blocking the generation of oxidants. The host's inability to eliminate H. pylori infection results in persistent ROS production. Notably, excessive ROS can disrupt the intracellular signal transduction and biological processes of the host, incurring chronic inflammation and cellular damage, such as DNA damage, lipid peroxidation, and protein oxidation. Markedly, the sustained inflammatory response and oxidative stress during H. pylori infection are major risk factor for gastric carcinogenesis. In this context, we summarize the literature on H. pylori infection‐induced ROS production, the strategies used by H. pylori to counteract the host response, and subsequent host damage and gastric carcinogenesis.

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Section: Host Damage and Gastric Cancermentioning

confidence: 99%

Section: Dna Damagementioning

confidence: 99%

Section: Dna Damagementioning

confidence: 99%

See 1 more Smart Citation

Reactive oxygen species and gastric carcinogenesis: The complex interaction between Helicobacter pylori and host

Wu,

Chen,

Chen

et al. 2023

Helicobacter

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AP endonuclease 1: Biological updates and advances in activity analysis

Almeida,

Andrews,

Sobol

2024

Methods in Enzymology

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Investigating the Effects of Chelidonic Acid on Oxidative Stress-Induced Premature Cellular Senescence in Human Skin Fibroblast Cells

Turkoglu,

Mansuroglu

2024

Life

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This study investigated the effects of chelidonic acid (CA) on hydrogen peroxide (H2O2) induced cellular senescence in human skin fibroblast cells (BJ). Cellular senescence is a critical mechanism that is linked to age-related diseases and chronic conditions. CA, a γ-pyrone compound known for its broad pharmacological activity, was assessed for its potential to mitigate oxidative stress and alter senescence markers. A stress-induced premature senescence (SIPS) model was designed in BJ fibroblast cells using the oxidative stress agent H2O2. After this treatment, cells were treated with CA, and the potential effect of CA on senescence was evaluated using senescence-related β-galactosidase, 4′,6-diamino-2-phenylindole (DAPI), acridine-orange staining (AO), comet assay, molecular docking assays, gene expression, and protein analysis. These results demonstrate that CA effectively reduces senescence markers, including senescence-associated β-galactosidase activity, DNA damage, lysosomal activity, and oxidative stress indicators such as malondialdehyde. Molecular docking revealed CA’s potential interactions with critical proteins involved in senescence signalling pathways, suggesting mechanisms by which CA may exert its effects. Gene expression and protein analyses corroborated the observed anti-senescent effects, with CA modulating p16, p21, and pRB1 expressions and reducing oxidative stress markers. In conclusion, CA appeared to have senolytic and senomorphic potential in vitro, which could mitigate and reverse SIPS markers in BJ fibroblasts.

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A Novel Hypomorphic Apex1 Mouse Model Implicates Apurinic/Apyrimidinic Endonuclease 1 in Oxidative DNA Damage Repair in Gastric Epithelial Cells

Cited by 3 publications

References 59 publications

Reactive oxygen species and gastric carcinogenesis: The complex interaction between Helicobacter pylori and host

Reactive oxygen species and gastric carcinogenesis: The complex interaction between Helicobacter pylori and host

AP endonuclease 1: Biological updates and advances in activity analysis

Investigating the Effects of Chelidonic Acid on Oxidative Stress-Induced Premature Cellular Senescence in Human Skin Fibroblast Cells

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