High expression of <scp>CD</scp>98 alters epithelial barrier functions to promote induction of airway allergy

Liu, T.; Ma, Jin; Li, T.-L.; Yang, Jie; Liang, Xiaofeng; Yang, Ping‐Chang

doi:10.1111/j.1365-2222.2012.03978.x

Cited by 11 publications

(8 citation statements)

References 23 publications

(29 reference statements)

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“…The epithelial barrier dysfunction occurs when macromolecular molecules, such as protein antigens, fail to pass through the epithelial barrier to arrive at the deep tissues of the body, such as the subepithelial region, where the antigens may contact various immune cells and initiate aberrant immune responses and immune inflammation. A number of factors are recognized associating with epithelial barrier dysfunction, including psychological stress (Zheng et al, ; Yu et al, ), exposure to microbial products (Li et al, ; Liu et al, ), allergy (Rezaee et al, ; Liu et al, ; Post et al, ) and chronic inflammation (Gersemann et al, ). To date, the underlying mechanism of epithelial barrier dysfunction is not fully understood.…”

Section: Introductionmentioning

confidence: 99%

Alphavbeta6 is required in maintaining the intestinal epithelial barrier function

Chen

et al. 2014

Cell Biology International

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Epithelial barrier dysfunction is involved in a large number of diseases, but the pathogenesis is unclear. Integrin alphavbeta6 (avb6) in involved in the maintenance of the mucosal homeostasis. We have investigated the role of avb6 in maintaining the epithelial barrier function. Using T84 monolayers cultures, transepithelial electric resistance (TER) and permeability to ovalbumin (OVA) were measured as indicators of functioning. The antigenicity of OVA collected from the Transwell basal chambers was assessed using OVA-specific T cell proliferation. Knockdown of the avb6 genes increased the permeability of T84 monolayers to OVA, but did not affect TER. The deficiency of avb6-related hyperpermeability in T84 monolayers could be compensated by adding exogenous avb6 to the culture. The OVA samples collected from the basal chambers had strong antigenicity as it markedly induced the antigen specific T cell proliferation. Addition of recombinant avb6 blocked increases in permeability of T84 monolayers to OVA induced by tumor necrosis factor-α.

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Section: Introductionmentioning

confidence: 99%

Alphavbeta6 is required in maintaining the intestinal epithelial barrier function

Chen

et al. 2014

Cell Biology International

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“…We have previously shown a dysregulation of miRNAs and protein expression levels along the ileal villus-crypt axis with a knockout of a single gene PepT1 , which codes for a peptide transporter in IEC, contributing to the molecular changes associated with cell death and proliferation 32 . The molecular and functional impact of a gene deletion, or gene overexpression as in current study, is highlighted by the comprehensive undertake in identifying miRNAs and proteins selectively affected by the target genes, potentially contributing to the changes in IE function 7 , 33 , 34 and inflammation 12 , 13 , 32 , 35 , 36 in experimental colitis.…”

Section: Discussionmentioning

confidence: 86%

Overexpression of CD98 in intestinal epithelium dysregulates miRNAs and their targeted proteins along the ileal villus-crypt axis

Han

Baker

Zhang

et al. 2018

Sci Rep

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CD98 has been implicated in the experimental model of inflammatory bowel disease. We have previously shown that IEC-specific overexpression of CD98 mediates intestinal inflammation and intestinal epithelial barrier dysfunction. Mice overexpressing CD98 exhibited severe colitis and a greater susceptibility to CAC. Here we demonstrated CD98 overexpression to dysregulate homeostatic gradient profile of miRNA and protein expression along the ileal villus-crypt axis. Using miRNA-target gene prediction module, we observed differentially expressed miRNAs to target proteins of villus and crypt profoundly affected by CD98 overexpression. We have utilized online bioinformatics as methods to further scrutinize the biological meanings of miRNA-target data. We identified significant interactions among the differentially regulated proteins targeted by altered miRNAs in Tg mice. The biological processes affected by the predicted targets of miRNAs deviate from the homeostatic functions of the miRNA-gene-protein axis of the wildtype mice. Our results emphasize a dynamic perturbation of miRNA and protein expression in villus-crypt axis contributing to potential biological consequences of altering CD98 expression. Our findings also suggest the need for a consideration of arrays of interacting biological entities (i.e. miRNAs-mRNAs, protein-protein interaction) or a combination comparison for a better understanding of the disease pathology which is necessary for an effective therapeutic target development.

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“…The pathogenesis of a number of diseases, such as allergic diseases [17] and chronic immune inflammation [18], are associated with the epithelial barrier dysfunction. Various factors, such as psychological stress, microbial infection and radiations, are suggested associated with the epithelial barrier dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Myosin VI contributes to maintaining epithelial barrier function

Liao

Jia

et al. 2013

J Biomed Sci

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BackgroundEpithelial barrier dysfunction is associated with the pathogenesis of a number of immune inflammations; the etiology is not fully understood. The fusion of endosome/lysosome is a critical process in the degradation of endocytic antigens in epithelial cells. Recent reports indicate that myosin VI (myo6) is involved in the activities of endosomes. The present study aims to investigate the role of myo6 in epithelial barrier dysfunction.ResultsThe endosome accumulation was observed in myo6-deficient Rmcs. More than 80% endosomes were fused with lysosomes in naïve Rmcs while less than 30% endosomes were fused with lysosomes in the myo6-deficient Rmcs. The myo6-deficient Rmc monolayers showed high permeability to a macromolecular antigen, ovalbumin, the latter still conserved the antigenicity, which induced strong T cell activation.ConclusionsWe conclude that myo6 plays a critical role in the fusion of endosome/lysosome in Rmc epithelial cells. Deficiency of myo6 compromises the epithelial barrier function.

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High expression of CD98 alters epithelial barrier functions to promote induction of airway allergy

Abstract: CD98 plays a critical role in compromising the airway epithelial barrier function that contributes to the induction of airway allergy.

Cited by 11 publications

References 23 publications

Alphavbeta6 is required in maintaining the intestinal epithelial barrier function

Alphavbeta6 is required in maintaining the intestinal epithelial barrier function

Overexpression of CD98 in intestinal epithelium dysregulates miRNAs and their targeted proteins along the ileal villus-crypt axis

Myosin VI contributes to maintaining epithelial barrier function

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