Expression of claudins in the normal canine gastric mucosa

Psáder, Roland; Jakab, Csaba; Máthé, Ákos; Balka, Gyula; Pápa, Kinga; Sterczer, Ágnes

doi:10.1556/avet.2013.053

Cited by 4 publications

(1 citation statement)

References 18 publications

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“…Studies by others have found a positive regulatory role of probiotic Lactobacillus casei or lactate on intestinal mucosal integrity, possibly by accelerating intestinal-stem-cell-mediated epithelial development [35,36]. Tight junction proteins are key factors contributing to the integrity of epithelial layers of the gastric mucus [31,37,38]. Using tight junction proteins as a proxy for gastric mucosal integrity, we found lactate could promote the expression of OCLN and CLDN-1, CLDN-5, but not that of TJP2, ZO-1 or CLDN-18.…”

Section: Discussionmentioning

confidence: 99%

Lactate as a metabolite from probiotic Lactobacilli mitigates ethanol-induced gastric mucosal injury: an in vivo study

Huang

Zhang

Dong

et al. 2021

BMC Complement Med Ther

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Background Pre-administration of probiotic Lactobacilli attenuates ethanol-induced gastric mucosal injury (GMI). The underpinning mechanisms remain to be elucidated. We speculated that lactate, the main metabolite of Lactobacillus that can be safely used as a common food additive, mediated the gastroprotective effect. This study aimed to gain experimental evidence to support our hypothesis and to shed lights on its underlying mechanisms. Methods Lactate was orally administrated to mice at different doses 30 min prior to the induction of GMI. Gastric tissue samples were collected and underwent histopathological and immunohistochemical assessments, enzyme-linked immunosorbent assay, quantitative polymerase chain reaction (qPCR) and western blot analyses. Results Pretreatment with lactate at 1–3 g/kg significantly curtailed the severity of ethanol-induced GMI, as shown by morphological and histopathological examinations of gastric tissue samples. Significantly lower level of cytokines indicative of local inflammation were found in mice receiving lactate treatment prior to ethanol administration. Western-blot, immunohistochemical analysis and qPCR suggested that gastroprotective properties of lactate were mediated by its modulatory effects on the expression of the apoptosis regulator gene Bax, the apoptotic executive protein gene Casp3, and genes critical for gastric mucosal integrity, including those encoding tight junction proteins Occludin, Claudin-1, Claudin-5, and that for lactate receptor GPR81. Conclusion Lactate mitigates ethanol-induced GMI by curtailing local gastric inflammatory response, down-regulating the expression of the apoptosis regulator and executor genes Bax and Casp3, and up-regulating the expression of genes encoding tight junction proteins Occludin, Claudin-1, and Claudin-5 and the lactate receptor GPR81.

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Section: Discussionmentioning

confidence: 99%

Lactate as a metabolite from probiotic Lactobacilli mitigates ethanol-induced gastric mucosal injury: an in vivo study

Huang

Zhang

Dong

et al. 2021

BMC Complement Med Ther

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Non-canonical functions of claudin proteins: Beyond the regulation of cell-cell adhesions

Hagen

2017

Tissue Barriers

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Tight junctions form a barrier to the diffusion of apical and basolateral membrane proteins thus regulating membrane polarity. They also regulate the paracellular movement of ions and water across epithelial and endothelial cells so that functionally they constitute an important permselective barrier. Permselectivity at tight junctions is regulated by claudins, which confer anion or cation permeability, and tightness or leakiness, by forming several highly regulated pores within the apical tight junction complex. One interesting feature of claudins is that they are, more often than not, localized to the basolateral membrane, in intracellular cytoplasmic vesicles, or in the nucleus rather than to the apical tight junction complex. These intracellular pools of claudin molecules likely serve important functions in the epithelium. This review will address the widespread prevalence of claudins that are not associated with the apical tight junction complex and discuss the important and emerging non-traditional functions of these molecules in health and disease.

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Tight junction disruption:Helicobacter pyloriand dysregulation of the gastric mucosal barrier

Caron¹

2015

WJG

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Long-term chronic infection with Helicobacter pylori (H. pylori) is a risk factor for gastric cancer development. In the multi-step process that leads to gastric cancer, tight junction dysfunction is thought to occur and serve as a risk factor by permitting the permeation of luminal contents across an otherwise tight mucosa. Mechanisms that regulate tight junction function and structure in the normal stomach, or dysfunction in the infected stomach, however, are largely unknown. Although conventional tight junction components are expressed in gastric epithelial cells, claudins regulate paracellular permeability and are likely the target of inflammation or H. pylori itself. There are 27 different claudin molecules, each with unique properties that render the mucosa an intact barrier that is permselective in a way that is consistent with cell physiology. Understanding the architecture of tight junctions in the normal stomach and then changes that occur during infection is important but challenging, because most of the reports that catalog claudin expression in gastric cancer pathogenesis are contradictory. Furthermore, the role of H. pylori virulence factors, such as cytotoxin-associated gene A and vacoulating cytotoxin, in regulating tight junction dysfunction during infection is inconsistent in different gastric cell lines and in vivo, likely because non-gastric epithelial cell cultures were initially used to unravel the details of their effects on the stomach. Hampering further study, as well, is the relative lack of cultured cell models that have tight junction claudins that are consistent with native tissues. This summary will review the current state of knowledge about gastric tight junctions, normally and in H. pylori infection, and make predictions about the consequences of claudin reorganization during H. pylori infection.

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Expression of claudins in the normal canine gastric mucosa

Cited by 4 publications

References 18 publications

Lactate as a metabolite from probiotic Lactobacilli mitigates ethanol-induced gastric mucosal injury: an in vivo study

Lactate as a metabolite from probiotic Lactobacilli mitigates ethanol-induced gastric mucosal injury: an in vivo study

Non-canonical functions of claudin proteins: Beyond the regulation of cell-cell adhesions

Tight junction disruption:Helicobacter pyloriand dysregulation of the gastric mucosal barrier

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