AMP-activated protein kinase activation protects gastric epithelial cells from Helicobacter pylori-induced apoptosis

Lv, Guoqiang; Zhu, Huanhuan; Zhou, Feng; Zhou, Lin; Lin, Gang; Li, Chenwan

doi:10.1016/j.bbrc.2014.09.028

Cited by 29 publications

(36 citation statements)

References 39 publications

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“…As previously reported [17], gastric biopsy specimens from the antral gastric mucosa were collected from adult patients undergoing esophagogastroduodenoscopy. The antral gastric mucosa were minced and incubated with 10 mM dithiothreitol and 1 mM EDTA at room temperature for 1 h with vigorous shaking.…”

Section: Human Gecs Isolation and Culturementioning

confidence: 99%

“…pylori 26695 [17] was maintained on blood agar plates (Becton Dickinson and Company, Franklin Lakes, NJ). H. pylori was added to GECs at a multiplicity of infection (MOI) of 100:1 and cocultured with GECs for the indicated times.…”

Section: H Pylori Culturementioning

confidence: 99%

“…An immortalized human GEC line [17], GES-1 cells were maintained in RPMI 1640 medium supplemented with 10% FBS (Gibco), with necessary antibiotics in a humidified atmosphere of 5% CO 2 .…”

Section: Ges-1 Cell Culturementioning

confidence: 99%

“…GEC apoptosis was detected by Annexin V Flow cytometry (FACS) assay, Histone-DNA enzyme-linked immunosorbent assay (ELISA) assay or terminal deoxynucleotidyl transferase dUTP nick end (TUNEL) staining assay as described [17].…”

Section: Apoptosis Assaymentioning

confidence: 99%

“…inhibit mammalian target of rapamycin (mTOR), and promotes cell survival under energy starvation conditions [15,16]. Our previous study identified that H. pylori-activated AMPK activation promotes GEC survival [17].…”

Section: Introductionmentioning

confidence: 99%

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Compound 13, an α1-selective small molecule activator of AMPK, inhibits Helicobacter pylori -induced oxidative stresses and gastric epithelial cell apoptosis

Zhao

Zhu

Zhou

et al. 2015

Biochemical and Biophysical Research Communications

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Section: Human Gecs Isolation and Culturementioning

confidence: 99%

Section: H Pylori Culturementioning

confidence: 99%

“…An immortalized human GEC line [17], GES-1 cells were maintained in RPMI 1640 medium supplemented with 10% FBS (Gibco), with necessary antibiotics in a humidified atmosphere of 5% CO 2 .…”

Section: Ges-1 Cell Culturementioning

confidence: 99%

Section: Apoptosis Assaymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Compound 13, an α1-selective small molecule activator of AMPK, inhibits Helicobacter pylori -induced oxidative stresses and gastric epithelial cell apoptosis

Zhao

Zhu

Zhou

et al. 2015

Biochemical and Biophysical Research Communications

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Additive interactions between PRKAA1 polymorphisms and Helicobacter pylori CagA infection associated with gastric cancer risk in Koreans

et al. 2016

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Although several studies reported genetic polymorphisms in protein kinase AMP‐activated alpha 1 catalytic subunit (PRKAA1) and their associations with gastric cancer risk, few have evaluated associations between Helicobacter pylori infection and PRKAA1 gene‐environment interactions. Here, we evaluated the effects of interactions between H. pylori infection and PRKAA1 polymorphisms on gastric cancer risk in Koreans. In this hospital‐based case–control study, PRKAA1 genotypes were analyzed and H. pylori infection and CagA status were examined using a serologic method in 846 pairs of gastric cancer patients and controls matched for age and sex. H. pylori seropositivity was associated with a 1.43‐fold [95% confidence interval: 1.12–1.81] increase in the risk of gastric cancer, and CagA low‐positive titers during H. pylori infection increased the risk by 1.85‐fold (95% confidence interval, 1.38–2.48). Significant positive interaction between the PRKAA1 rs13361707 genotype and H. pylori infection was verified on an additive scale [relative excess risk due to interaction, 0.55; 95% confidence interval, 0.05–1.04; P = 0.030], and the gene‐environment interaction between PRKAA1 rs13361707 and CagA status was also statistically significant (relative excess risk due to interaction, 0.50; 95% confidence interval, 0.30–0.70; P < 0.001). Our results indicated that H. pylori infection, CagA status, and PRKAA1 polymorphisms were risk factors for gastric cancer in Koreans, and that the combination of two of these factors rather than their independent effects synergistically increased the risk.

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PRKAA1 rs13361707 C/T polymorphism confers decreased susceptibility to esophageal cancer: A case‐control study

Zhao

Zang

2020

Clinical Laboratory Analysis

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Background Several studies probed into the connection between esophageal cancer (EC) risk and PRKAA1 rs13361707 C/T polymorphism, but obtained insignificant findings. Methods In this study, 814 EC cases and 961 controls from Eastern China were recruited to validate the relationship between this polymorphism and EC susceptibility. Results Data suggested rs13361707 C/T polymorphism in PRKAA1 gene was significantly related with a lower risk for EC. Such significant connection was also uncovered in subgroups of males, smokers, drinkers and individuals with age ≥ 60 years. In addition, this polymorphism was linked with the pathological grading, distant metastasis, and histology of EC. Conclusion In summary, PRKAA1 rs13361707 C/T polymorphism is related to the risk and clinical properties of EC patients in East China.

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AMP-activated protein kinase activation protects gastric epithelial cells from Helicobacter pylori-induced apoptosis

Cited by 29 publications

References 39 publications

Compound 13, an α1-selective small molecule activator of AMPK, inhibits Helicobacter pylori -induced oxidative stresses and gastric epithelial cell apoptosis

Compound 13, an α1-selective small molecule activator of AMPK, inhibits Helicobacter pylori -induced oxidative stresses and gastric epithelial cell apoptosis

Additive interactions between PRKAA1 polymorphisms and Helicobacter pylori CagA infection associated with gastric cancer risk in Koreans

PRKAA1 rs13361707 C/T polymorphism confers decreased susceptibility to esophageal cancer: A case‐control study

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