Delayed Disruption of Barrier Function in Cultured Human Corneal Epithelial Cells Induced by Tumor Necrosis Factor-α in a Manner Dependent on NF-κB

Kimura, Kazuhiro; Teranishi, Shinichiro; Fukuda, Ken; Kawamoto, Koji; Nishida, Teruo

doi:10.1167/iovs.07-0419

Cited by 92 publications

(65 citation statements)

References 57 publications

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“…There may be evidence to support the proposition that corneal epithelial barrier function could be compromised by higher levels of shear stress in the Asian eye. For example, mechanical insult to the cornea induced by shear stress may be responsible for epithelial cell apoptosis, desquamation, and disruption of tight junctions [35][36][37][38][39] and has been implicated as a contributing factor to the inflammatory response associated with dry eye [40,41], these factors are likely responsible for increased corneal epithelial permeability. Shear stress-induced epithelial surface disruption and inflammation could explain recent studies reporting greater prevalence of dry eye in Asians compared with non-Asians [42][43][44].…”

Section: Discussionmentioning

confidence: 99%

Corneal epithelial permeability: Ethnic differences between Asians and non-Asians

Li¹,

Hsiao²,

Graham³

et al. 2013

Contact Lens and Anterior Eye

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a b s t r a c tPurpose: To ascertain whether a difference in the permeability of the corneal epithelium to fluorescein (P dc ) exists between Asians and non-Asians. Methods: From a multi-study database we extracted 632 records of baseline, open-eye P dc measurements taken on both eyes of 176 subjects. Subjects were awake for a minimum of 4 h before measurement, and were free of ocular disease and central corneal staining. P dc was transformed by natural logarithm to better approximate normality for statistical tests. Results: The mean ln(P dc ) in the Asian group was significantly greater than in the non-Asian group [−2.34 ln(nm/s) vs. −2.58 ln(nm/s); p < 0.001]. Conclusions: Compared with non-Asians, Asians exhibited a less negative ln(P dc ), which translates to a higher P dc and a more permeable corneal epithelium. We speculate that this may be related to anatomic differences responsible for greater eyelid tension in Asians.

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Section: Discussionmentioning

confidence: 99%

Corneal epithelial permeability: Ethnic differences between Asians and non-Asians

Li¹,

Hsiao²,

Graham³

et al. 2013

Contact Lens and Anterior Eye

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“…Ma and co-workers have shown that the TNFa-induced increase in TJ permeability of Caco-2 cells was associated with a downregulation of ZO-1 protein expression, which was accompanied by an altered tight junction localization of ZO-1, and this was prevented by NFkB inhibitors (Ma et al, 2004). In corneal epithelial cells, TNFa disrupted the barrier function of HCE cells, with a disappearance of ZO-1 at TJs resulting in a decrease of R t , whereas the NFkB inhibitor curcumin blocked these effects of TNFa on R t and the subcellular localization of ZO-1 (Soler et al, 1999;Kimura et al, 2008). It has been hypothesized that the activation of NFkB can induce transcription and translation of certain target genes, which subsequently lead to the inhibition of TJ protein expression.…”

Section: Fig 6 Specific Blockers In Tnfa-and Berberine-induced Tj Rmentioning

confidence: 99%

TNFα-induced and berberine-antagonized tight junction barrier impairment via tyrosine kinase, Akt and NFκB signaling

Amasheh

Fromm

Krug

et al. 2010

Journal of Cell Science

198

143

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SummaryTNFa-mediated tight junction defects contribute to diarrhea in inflammatory bowel diseases (IBDs). In our study, the signaling pathways of the TNFa effect on barrier-or pore-forming claudins were analyzed in HT-29/B6 human colon monolayers. Berberine, a herbal therapeutic agent that has been recently established as a therapy for diabetes and hypercholesterinemia, was able to completely antagonize the TNFa-mediated barrier defects in the cell model and in rat colon. Ussing chamber experiments and two-path impedance spectroscopy revealed a decrease of paracellular resistance after TNFa to 11±4%, whereas transcellular resistance was unchanged. The permeability of the paracellular marker fluorescein was increased fourfold. Berberine alone had no effect while it fully prevented the TNFa-induced barrier defects. This effect on resistance was confirmed in rat colon. TNFa removed claudin-1 from the tight junction and increased claudin-2 expression. Berberine prevented TNFa-induced claudin-1 disassembly and upregulation of claudin-2. The effects of berberine were mimicked by genistein plus BAY11-7082, indicating that they are mediated via tyrosine kinase, pAkt and NFkB pathways. In conclusion, the anti-diarrheal effect of berberine is explained by a novel mechanism, suggesting a therapeutic approach against barrier breakdown in intestinal inflammation.

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“…22,23 Furthermore, another in vitro study using the NF-B inhibitor curcumin indicated that barrier function and subcellular localization of zona occludens (ZO)-1 is dependent on NF-B following TNF-␣ administration. 24 Interestingly, results in epithelial-specific IKK knockout mice showed that colitis-induced cell proliferation was unaffected while crypt cell apoptosis increased in the absence of NF-B signaling. 25 These studies highlight the importance of using site-specific models of NF-B-deficient signaling to understand NF-B biology in the intestine.…”

mentioning

confidence: 99%

Epithelial NF-κB Enhances Transmucosal Fluid Movement by Altering Tight Junction Protein Composition after T Cell Activation

Tang¹,

Clayburgh

Mittal³

et al. 2010

The American Journal of Pathology

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In inflammatory bowel disease (IBD) , aberrant activation of innate and adaptive immune responses enhances mucosal permeability through mechanisms not completely understood. To examine the role of epithelial nuclear factor (NF-B) in IBD-induced enhanced permeability , epithelial-specific IB␣ mutant (NF-B super repressor) transgenic (TG) mice were generated. NF-kB activation was inhibited in TG mice, relative to wild-type mice , following T cell-mediated immune cell activation using an anti-CD3 monoclonal antibody. Furthermore , epithelial NF-B super repressor protein inhibited diarrhea and blocked changes in transepithelial resistance and transmucosal flux of alexa350 (0.35 kDa) and dextran3000 (3 kDa). In vivo perfusion loop studies in TG mice revealed reversed net water secretion and reduced lumenal flux of different molecular probes (bovine serum albumin, alexa350, and dextran3000). Cell-imaging and immunoblotting of low-density, detergent-insoluble membrane fractions confirmed that tight junction proteins (occludin, claudin-1 and zona occludens-1) are internalized through an NF-B-dependent pathway. Taken together, these data suggest that IBD-associated diarrhea results from NF-B-mediated tight junction protein internalization and increased paracellular permeability. Thus, reduction of epithelial NF-B activation in IBD may repair defects in epithelial barrier function, reduce diarrhea, and limit protein (eg, serum albumin) losses. Epithelial NF-B activation induced by mucosal T cells, therefore, actively plays a role in opening paracellular spaces to promote transmucosal fluid effux into the intestinal lumen.

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Delayed Disruption of Barrier Function in Cultured Human Corneal Epithelial Cells Induced by Tumor Necrosis Factor-α in a Manner Dependent on NF-κB

Abstract: TNF-alpha disrupted the barrier function of HCE cells, apparently by affecting the localization of ZO-1 at TJs in a manner dependent on NF-kappaB at late phase. This action of TNF-alpha may contribute to the loss of corneal epithelial barrier function associated with ocular inflammation.

Cited by 92 publications

References 57 publications

Corneal epithelial permeability: Ethnic differences between Asians and non-Asians

Corneal epithelial permeability: Ethnic differences between Asians and non-Asians

TNFα-induced and berberine-antagonized tight junction barrier impairment via tyrosine kinase, Akt and NFκB signaling

Epithelial NF-κB Enhances Transmucosal Fluid Movement by Altering Tight Junction Protein Composition after T Cell Activation

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