Do mild irritants protect surface epithelial cells of gastric mucosa against ethanol-induced damage in rat? an ultrastructural study of adaptive cytoprotection

1989 ◽  
Vol 24 (1) ◽  
pp. 80-80
Author(s):  
A. Terano ◽  
J. Shiga ◽  
H. Hiraishi ◽  
S. Ota ◽  
H. Mutdh ◽  
...  
Keyword(s):  
Gastric Mucosa ◽  
Epithelial Cells ◽  
Ultrastructural Study ◽  
Adaptive Cytoprotection ◽  
Mild Irritants

Nonprotein sulfhydryl compounds in canine gastric mucosa: effects of PGE2 and ethanol

1985 ◽  
Vol 249 (1) ◽  
pp. G137-G144 ◽  
Author(s):  
T. A. Miller ◽  
D. Li ◽  
Y. J. Kuo ◽  
K. L. Schmidt ◽  
L. L. Shanbour
Keyword(s):  
Gastric Mucosa ◽  
Low Dose ◽  
Mucosal Damage ◽  
Gastric Mucosal Damage ◽  
High Dose ◽  
Mucosal Protection ◽  
Gastric Mucosal Protection ◽  
Sulfhydryl Compounds ◽  
Mild Irritants

By use of an in vivo canine chambered stomach preparation in which the gastric mucosa was partitioned into two equal halves, the effect of topical 16,16-dimethyl PGE2 (DMPGE2) (1 microgram/ml of perfusate) and 8% and 40% ethanol on tissue levels of nonprotein sulfhydryl compounds was assessed. Both DMPGE2 and 8% ethanol significantly increased (P less than 0.005) mucosal levels of nonprotein sulfhydryls when compared with corresponding mucosa bathed with saline alone. In contrast, mucosa bathed with 40% ethanol showed significantly decreased levels. If mucosa was bathed with DMPGE2 or 8% ethanol prior to exposing the stomach to 40% ethanol, this depletion in sulfhydryl compounds was not observed. Since other experimental observations have shown that exogenously administered prostaglandins and mild irritants (such as low-dose alcohol) can prevent gastric mucosal damage by necrotizing agents (such as high-dose alcohol), our findings are consistent with the hypothesis that nonprotein sulfhydryls may play a role in mediating gastric mucosal protection.

scholarly journals Autophagy protects gastric mucosal epithelial cells from ethanol-induced oxidative damage via mTOR signaling pathway

2017 ◽  
Vol 242 (10) ◽  
pp. 1025-1033 ◽  
Author(s):  
Weilong Chang ◽  
Jie Bai ◽  
Shaobo Tian ◽  
Muyuan Ma ◽  
Wei Li ◽  
...  
Keyword(s):  
Gastric Mucosa ◽  
Epithelial Cells ◽  
Oxidative Damage ◽  
Signaling Pathway ◽  
Cell Damage ◽  
Mtor Signaling ◽  
Adaptive Mechanism ◽  
Mtor Signaling Pathway ◽  
Mucosal Epithelial Cell ◽  
Ethanol Toxicity

Alcohol abuse is an important cause of gastric mucosal epithelial cell injury and gastric ulcers. A number of studies have demonstrated that autophagy, an evolutionarily conserved cellular mechanism, has a protective effect on cell survival. However, it is not known whether autophagy can protect gastric mucosal epithelial cells against the toxic effects of ethanol. In the present study, gastric mucosal epithelial cells (GES-1 cells) and Wistar rats were treated with ethanol to detect the adaptive response of autophagy. Our results demonstrated that ethanol exposure induced gastric mucosal epithelial cell damage, which was accompanied by the downregulation of mTOR signaling pathway and activation of autophagy. Suppression of autophagy with pharmacological agents resulted in a significant increase of GES-1 cell apoptosis and gastric mucosa injury, suggesting that autophagy could protect cells from ethanol toxicity. Furthermore, we evaluated the cellular oxidative stress response following ethanol treatment and found that autophagy induced by ethanol inhibited generation of reactive oxygen species and degradation of antioxidant and lipid peroxidation. In conclusion, these findings provide evidence that ethanol can activate autophagy via downregulation of the mTOR signaling pathway, serving as an adaptive mechanism to ameliorate oxidative damage induced by ethanol in gastric mucosal epithelial cells. Therefore, modifying autophagy may provide a therapeutic strategy against alcoholic gastric mucosa injury. Impact statement The effect and mechanism of autophagy on ethanol-induced cell damage remain controversial. In this manuscript, we report the results of our study demonstrating that autophagy can protect gastric mucosal epithelial cells against ethanol toxicity in vitro and in vivo. We have shown that ethanol can activate autophagy via downregulation of the mTOR signaling pathway, serving as an adaptive mechanism to ameliorate ethanol-induced oxidative damage in gastric mucosal epithelial cells. This study brings new and important insights into the mechanism of alcoholic gastric mucosal injury and may provide an avenue for future therapeutic strategies.

scholarly journals microRNA-29a-3p, Up-Regulated in Human Gastric Cells and Tissues with H.Pylori Infection, Promotes the Migration of GES-1 Cells via A20-Mediated EMT Pathway

2018 ◽  
Vol 51 (3) ◽  
pp. 1250-1263 ◽  
Author(s):  
Fengying Sun ◽  
Ying Ni ◽  
Hong Zhu ◽  
Jian Fang ◽  
Hua Wang ◽  
...  
Keyword(s):  
Gastric Mucosa ◽  
Epithelial Cells ◽  
Western Blotting ◽  
Molecular Mechanisms ◽  
Luciferase Reporter ◽  
Human Gastric Mucosa ◽  
Gastric Epithelial Cells ◽  
Migration Ability ◽  
Gastric Cells ◽  
Dose Dependent

Background/Aims: Helicobacter pylori (H. pylori) infection is closely related to human gastric mucosa-associated diseases. Several recent studies on miRNAs have expanded our insights on H.pylori pathogenesis. This study aimed to investigate the biological roles and underlying molecular mechanisms of miR-29a-3p in human gastric cells and tissues with H.pylori infection. Methods: miR-29a-3p expression was quantified by quantitative RT-PCR (qRT-PCR). A miR-29a-3p target gene was validated by bioinformatics analysis, western blotting and dual luciferase reporter gene assays. Western blotting and immunohistochemistry (IHC) assay were performed to detect the protein expression. Transwell assay was used to determine the cell migration ability. Results: MiR-29a-3p was up-regulated in H.pylori-positive gastric mucosa tissues and H.pylori-infected gastric cells. The up-regulation of miR-29a-3p was dose-dependent in BGC-823 and GES-1 cells infected with H.pylori. Using gain- and loss-of-function experiments in vitro, we demonstrated that miR-29a-3p promoted the migration of gastric epithelial cells. We further characterized A20 as a direct target of miR-29a-3p. The expression of A20 was decreased in H.pylori-positive gastric mucosa tissues compared with H.pylori-negative gastric mucosa tissues. A20 downregulation was time- and dose-dependent in GES-1 and BGC-823 cells infected with H.pylori. In GES-1 and BGC-823 cells infected with H.pylori, the miR-29a-3p mimic significantly blocked A20 expression, which suggests that H.pylori decreased A20 expression through up-regulating miR-29a-3p in GES-1 and BGC-823 cells infected with H.pylori. The knockdown of A20 by siRNA enhanced the migration of human gastric epithelial cells and promoted the expression of Snail, Vimentin, and N-cadherin and inhibited the expression of E-cadherin. Conclusion: The miR-29a-3p may act as a tumor promotive miRNA by regulating cells migration through directly targeting of A20 gene in human gastric epithelial cells infected with H.pylori.

Macrophages and epithelial cells of the thymus gland. An ultrastructural study in the natterjack, Bufo calamita

1989 ◽  
Vol 21 (1) ◽  
pp. 69-81 ◽  
Author(s):  
M.G. Barrutia ◽  
M. Torroba ◽  
M.J. Fernandez ◽  
A. Vicente ◽  
A.G. Zapata
Keyword(s):  
Epithelial Cells ◽  
Ultrastructural Study ◽  
Thymus Gland ◽  
Bufo Calamita

Secretin regulates paracellular permeability in canine gastric monolayers by a Src kinase-dependent pathway

2002 ◽  
Vol 283 (4) ◽  
pp. G893-G899 ◽  
Author(s):  
Monica C. Chen ◽  
Travis E. Solomon ◽  
Eduardo Perez Salazar ◽  
Robert Kui ◽  
Enrique Rozengurt ◽  
...  
Keyword(s):  
Gastric Mucosa ◽  
Epithelial Cells ◽  
Tyrosine Kinase ◽  
Tyrosine Kinase Inhibitor ◽  
Tyrosine Phosphorylation ◽  
Molecular Mechanisms ◽  
Kinase Inhibitor ◽  
Paracellular Permeability ◽  
Maximal Response ◽  
Src Tyrosine Kinase

Previous studies found that epidermal growth factor (EGF) decreased paracellular permeability in gastric mucosa, but the other physiological regulators and the molecular mechanisms mediating these responses remain undefined. We investigated the role of secretin and Src in regulating paracellular permeability because secretin regulates gastric chief cell function and Src mediates events involving the cytoskeletal-membrane interface, respectively. Confluent monolayers were formed from canine gastric epithelial cells in short-term culture on Transwell filter inserts. Resistance was monitored in the presence of secretin with or without specific kinase inhibitors. Tyrosine phosphorylation of Src at Tyr416 was measured with a site-specific phosphotyrosine antibody. Basolateral, but not apical, secretin at concentrations from 1 to 100 nM dose dependently increased resistance; this response was rapid and sustained over hours. PP2 (10 μM), a selective Src tyrosine kinase inhibitor, but not the inactive isomer PP3, abolished the increase in resistance by secretin but only modestly attenuated apical EGF effects. AG-1478 (100 nM), a specific EGF receptor tyrosine kinase inhibitor, attenuated the resistance increase to EGF but not secretin. Secretin, but not EGF, induced tyrosine phosphorylation of Src at Tyr416 in a dose-dependent fashion, with the maximal response observed at 1 min. PP2, but not PP3, dramatically inhibited this tyrosine phosphorylation. Secretin increases paracellular resistance in gastric mucosa through a Src-mediated pathway, while the effect of EGF is Src independent. Src appears to mediate the physiological effects of this Gs-coupled receptor in primary epithelial cells.

scholarly journals Expression of claudins in the normal canine gastric mucosa

2014 ◽  
Vol 62 (1) ◽  
pp. 13-21 ◽  
Author(s):  
Roland Psáder ◽  
Csaba Jakab ◽  
Ákos Máthé ◽  
Gyula Balka ◽  
Kinga Pápa ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Gastric Mucosa ◽  
Epithelial Cells ◽  
Apical Part ◽  
Basal Part ◽  
Gastric Epithelial Cells ◽  
Gastric Glands ◽  
Gastric Cells ◽  
Pyloric Stomach ◽  
Mucous Neck Cells

The aim of the present study was to investigate the expression pattern of claudin-1, -2, -3, -4, -5, -7, -8, -10 and -18 in the intact fundic and pyloric gastric mucosa of dogs. Intense, linear, membranous claudin-18 positivity was detected in the surface gastric cells and in the epithelial cells of the gastric glands both in the fundic and pyloric stomach regions. The mucous neck cells in the apical part of the glands, furthermore the parietal cells and chief cells of the basal part of the gland were all positive for claudin-18, in the same way as the enteroendocrine cells. Cells of the basal part of the pyloric glands showed intense, linear, membranous claudin-2 positivity, but cells of the superficial portion of these glands and the surface gastric cells in this region were claudin-2 negative. Fibroblasts, endothelial cells, lymphocytes of the propria layer, smooth muscle cells and vegetative neurons were all negative for claudin-2. All gastric epithelial cells were negative for claudin-1, -3, -4, -5, -6, -7, -8 and -10. The endothelial cells of the propria layer had intense claudin-5 positivity. We assume that claudin-18 forms a paracellular barrier against gastric acid in the healthy canine stomach, in the same way as in mice.

scholarly journals Single-cell transcriptional analyses of spasmolytic polypeptide-expressing metaplasia arising from acute drug injury and chronic inflammation in the stomach

Gut ◽  
2019 ◽  
Vol 69 (6) ◽  
pp. 1027-1038 ◽  
Author(s):  
Kevin A Bockerstett ◽  
Scott A Lewis ◽  
Kyle J Wolf ◽  
Christine N Noto ◽  
Nicholas M Jackson ◽  
...  
Keyword(s):  
Gastric Mucosa ◽  
Epithelial Cells ◽  
Single Cell ◽  
Chronic Inflammation ◽  
Intrinsic Factor ◽  
Drug Induced ◽  
Cell Hyperplasia ◽  
Tissue Samples ◽  
Spasmolytic Polypeptide ◽  
The Individual

ObjectiveSpasmolytic polypeptide-expressing metaplasia (SPEM) is a regenerative lesion in the gastric mucosa and is a potential precursor to intestinal metaplasia/gastric adenocarcinoma in a chronic inflammatory setting. The goal of these studies was to define the transcriptional changes associated with SPEM at the individual cell level in response to acute drug injury and chronic inflammatory damage in the gastric mucosa.DesignEpithelial cells were isolated from the gastric corpus of healthy stomachs and stomachs with drug-induced and inflammation-induced SPEM lesions. Single cell RNA sequencing (scRNA-seq) was performed on tissue samples from each of these settings. The transcriptomes of individual epithelial cells from healthy, acutely damaged and chronically inflamed stomachs were analysed and compared.ResultsscRNA-seq revealed a population Mucin 6 (Muc6)+gastric intrinsic factor (Gif)+ cells in healthy tissue, but these cells did not express transcripts associated with SPEM. Furthermore, analyses of SPEM cells from drug injured and chronically inflamed corpus yielded two major findings: (1) SPEM and neck cell hyperplasia/hypertrophy are nearly identical in the expression of SPEM-associated transcripts and (2) SPEM programmes induced by drug-mediated parietal cell ablation and chronic inflammation are nearly identical, although the induction of transcripts involved in immunomodulation was unique to SPEM cells in the chronic inflammatory setting.ConclusionsThese data necessitate an expansion of the definition of SPEM to include Tff2+Muc6+ cells that do not express mature chief cell transcripts such as Gif. Our data demonstrate that SPEM arises by a highly conserved cellular programme independent of aetiology and develops immunoregulatory capabilities in a setting of chronic inflammation.

Sign in / Sign up

Export Citation Format

Share Document