Differential expression of miRNA-146a and miRNA-155 in gastritis induced by Helicobacter pylori infection in paediatric patients, adults, and an animal model

Cortés-Márquez, Ana Caren; Mendoza-Elizalde, Sandra; Arenas-Huertero, Francisco; Trillo-Tinoco, Jimena; Valencia-Mayoral, Pedro; Consuelo-Sánchez, Alejandra; Zarate-Franco, Jonathan; Dionicio-Avendaño, Ada Ruth; Herrera-Esquivel, José de Jesús; Recinos-Carrera, E G; Colín-Valverde, Christian; Rivera-Gutierrez, Sandra; Reyes‐López, Alfonso; Vigueras-Galindo, J.C.; Velázquez-Guadarrama, Norma

doi:10.1186/s12879-018-3368-2

Cited by 29 publications

(29 citation statements)

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“…A recent study revealed the upregulation of miR-146a and miR-155 in patients with gastritis induced by H. pylori infection[13], with the similar findings demonstrated by another research group[14]. Cortés-Márquez et al[14] further grouped the patients with gastritis by age, and found that both children and adults with H. pylori -induced gastritis displayed higher levels of miR-145a and miR-155. Moreover, the cancerization tendency of H. pylori -induced gastritis was correlated with the upregulation of miR-146a and miR-155[13,14].…”

Section: Introductionsupporting

confidence: 55%

“…MiRNAs have no ability to encode proteins, but contribute to the modulation of gene expression[11,12]. A recent study revealed the upregulation of miR-146a and miR-155 in patients with gastritis induced by H. pylori infection[13], with the similar findings demonstrated by another research group[14]. Cortés-Márquez et al[14] further grouped the patients with gastritis by age, and found that both children and adults with H. pylori -induced gastritis displayed higher levels of miR-145a and miR-155.…”

Section: Introductionmentioning

confidence: 70%

“…Cortés-Márquez et al[14] further grouped the patients with gastritis by age, and found that both children and adults with H. pylori -induced gastritis displayed higher levels of miR-145a and miR-155. Moreover, the cancerization tendency of H. pylori -induced gastritis was correlated with the upregulation of miR-146a and miR-155[13,14]. In addition, H. pylori infection could result in the downregulation of miRNAs.…”

Section: Introductionmentioning

confidence: 99%

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MiR-32-5p aggravates intestinal epithelial cell injury in pediatric enteritis induced by Helicobacter pylori

Feng¹,

Guo²,

Wang³

et al. 2019

WJG

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BACKGROUNDPediatric enteritis is one of the infectious diseases in the digestive system that causes a variety of digestive problems, including diarrhea, vomiting, and bellyache in children. Clinically, Helicobacter pylori (H. pylori) infection is one of the common factors to cause pediatric enteritis. It has been demonstrated that aberrant expression of microRNAs (miRNAs) is found in gastrointestinal diseases caused by H. pylori, and we discovered a significant increase of miR-32-5p in H. pylori-related pediatric enteritis. However, the exact role of miR-32-5p in it is still unknown.AIMTo investigate the role of aberrant miR-32-5p in pediatric enteritis induced by H. pylori.METHODSMiR-32-5p expression was detected by quantitative real time-polymerase chain reaction. The biological role of miR-32-5p in H. pylori-treated intestinal epithelial cells was evaluated by Cell Counting Kit-8 assay and flow cytometry. The potential target of miR-32-5p was predicted with TargetScanHuman and verified by luciferase assay. The downstream mechanism of miR-32-5p was explored by using molecular biology methods.RESULTSWe found that miR-32-5p was overexpressed in serum of H. pylori-induced pediatric enteritis. Further investigation revealed that H. pylori infection promoted the death of intestinal epithelial cells, and increased miR-32-5p expression. Moreover, miR-32-5p mimic further facilitated apoptosis and inflammatory cytokine secretion of intestinal epithelial cells. Further exploration revealed that SMAD family member 6 (SMAD6) was the direct target of miR-32-5p, and SMAD6 overexpression partially rescued cell damage induced by H. pylori. The following experiments showed that miR-32-5p/SMAD6 participated in the apoptosis of intestinal epithelial cells induced by transforming growth factor-β-activated kinase 1 (TAK1)-p38 activation under H. pylori infection.CONCLUSIONOur work uncovered the crucial role of aberrant expression of miR-32-5p in H. pylori–related pediatric enteritis, and suggested that the TAK1-p38 pathway is involved in it.

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Section: Introductionsupporting

confidence: 55%

Section: Introductionmentioning

confidence: 70%

Section: Introductionmentioning

confidence: 99%

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MiR-32-5p aggravates intestinal epithelial cell injury in pediatric enteritis induced by Helicobacter pylori

Feng¹,

Guo²,

Wang³

et al. 2019

WJG

View full text Add to dashboard Cite

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“…miRNA-146a and miRNA-155 have been described as downregulated in GC (Hou et al, 2012;Li et al, 2012), but also as a potential oncogenes in vitro (Shomali et al, 2017;Qu et al, 2018). Cortés-Márquez et al (2018) described higher gastric expression in both miRNAs in children, especially in those with severe gastritis, as observed in adults and in animal models. Because their role in carcinogenesis is controversial, further studies are needed to determine the potential role of overexpression among infected children.…”

Section: Micro Rnasmentioning

confidence: 97%

Gastric Damage and Cancer-Associated Biomarkers in Helicobacter pylori-Infected Children

et al. 2020

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Helicobacter pylori (H. pylori) is well-known to be involved in gastric carcinogenesis, associated with deregulation of cell proliferation and epigenetic changes in cancerrelated genes. H. pylori infection is largely acquired during childhood, persisting long-term in about half of infected individuals, a subset of whom will go on to develop peptic ulcer disease and eventually gastric cancer, however, the sequence of events leading to disease is not completely understood. Knowledge on carcinogenesis and gastric damage-related biomarkers is abundant in adult populations, but scarce in children. We performed an extensive literature review focusing on gastric cancer related biomarkers identified in adult populations, which have been detected in children infected with H. pylori. Biomarkers were related to expression levels (RNA or protein) and/or methylation levels (DNA) in gastric tissue or blood of infected children as compared to non-infected controls. In this review, we identified 37 biomarkers of which 24 are over expressed, three are under expressed, and ten genes are significantly hypermethylated in H. pylori-infected children compared to healthy controls in at least 1 study. Only four of these biomarkers (pepsinogen I, pepsinogen II, gastrin, and SLC5A8) have been studied in asymptomatically infected children. Importantly, 13 of these biomarkers (β-catenin, C-MYC, GATA-4, DAPK1, CXCL13, DC-SIGN, TIMP3, EGFR, GRIN2B, PIM2, SLC5A8, CDH1, and VCAM-1.) are consistently deregulated in infected children and in adults with gastric cancer. Future studies should be designed to determine the clinical significance of these changes in infection-associated biomarkers in children and their persistence over time. The effect of eradication therapy over these biomarkers in children if proven significant, could lead to modifications in treatment guidelines for younger populations, and eventually promote the development of preventive strategies, such as vaccination, in the near future.

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“…MiRNA‐155 is a crucial regulator of innate immunity and is expressed in a variety of immune cells during the inflammatory response. Cortes‐Marquez et al analyzed for the first time the expression of miRNAs associated with H pylori infection in pediatric patients. The results showed that increased expression of miRNA‐146a and miRNA‐155 was associated with the duration and outcome of H pylori infection, suggesting that different expression of miRNAs is indicative of the chronicity of infection and disease severity.…”

Section: Pathophysiologymentioning

confidence: 99%

Review: Helicobacter pylori in pediatrics

2019

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Despite a decrease in the prevalence of Helicobacter pylori infection, it still poses a significant health burden worldwide. This review summarizes important pediatric studies on H pylori published from April 2018 to March 2019. Epidemiologic studies have reported different prevalences in different parts of the world and have mainly confirmed traditional risk factors. Several studies on pathophysiology attempted to identify risk markers in childhood for gastric cancer development later in life. One of the most interesting studies evaluated the relationship between eosinophilic esophagitis and H pylori infection; however, an inverse relationship was not confirmed. The high resistance of H pylori and, consequently, low eradication rates, is still a major concern and susceptibility testing before treatment has again been highlighted. Potassium‐competitive acid blockers are promising new acid‐suppressant drugs but their role in H pylori eradication schemes is still to be determined.

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Differential expression of miRNA-146a and miRNA-155 in gastritis induced by Helicobacter pylori infection in paediatric patients, adults, and an animal model

Cited by 29 publications

References 40 publications

MiR-32-5p aggravates intestinal epithelial cell injury in pediatric enteritis induced by Helicobacter pylori

MiR-32-5p aggravates intestinal epithelial cell injury in pediatric enteritis induced by Helicobacter pylori

Gastric Damage and Cancer-Associated Biomarkers in Helicobacter pylori-Infected Children

Review: Helicobacter pylori in pediatrics

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