Functional coupling of tight junctions and microfilaments in T84 monolayers

Madara, James L.; Stafford, J; Barenberg, David; Carlson, Susan

doi:10.1152/ajpgi.1988.254.3.g416

Cited by 98 publications

(103 citation statements)

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“…Previous studies have shown that cytochalasins and Na ϩ -glucose co-transporter induced increase in intestinal TJ permeability in vitro and in vivo was triggered by MLCK-induced increase in MLC phosphorylation (42,56,57). MLC phosphorylation then leads to an energy-dependent contraction of peri-junctional acto-myosin filaments, and mechanical tension induced retraction of junctional membrane and TJ proteins, and functional opening of the TJ barrier (40,57,60). The over-expression of constitutively active MLCK has also been shown to cause MLC phosphorylation and functional opening of the TJ barrier in MDCK cells (45).…”

Section: Discussionmentioning

confidence: 99%

Mechanism of IL-1β-Induced Increase in Intestinal Epithelial Tight Junction Permeability

Al–Sadi

Dokładny

et al. 2008

The Journal of Immunology

371

295

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The IL-1β-induced increase in intestinal epithelial tight junction (TJ) permeability has been postulated to be an important mechanism contributing to intestinal inflammation of Crohn’s disease and other inflammatory conditions of the gut. The intracellular and molecular mechanisms that mediate the IL-1β-induced increase in intestinal TJ permeability remain unclear. The purpose of this study was to elucidate the mechanisms that mediate the IL-1β-induced increase in intestinal TJ permeability. Specifically, the role of myosin L chain kinase (MLCK) was investigated. IL-1β caused a progressive increase in MLCK protein expression. The time course of IL-1β-induced increase in MLCK level correlated linearly with increase in Caco-2 TJ permeability. Inhibition of the IL-1β-induced increase in MLCK protein expression prevented the increase in Caco-2 TJ permeability. Inhibition of the IL-1β-induced increase in MLCK activity also prevented the increase in Caco-2 TJ permeability. Additionally, knock-down of MLCK protein expression by small interference RNA prevented the IL-1β-induced increase in Caco-2 TJ permeability. The IL-1β-induced increase in MLCK protein expression was preceded by an increase in MLCK mRNA expression. The IL-1β-induced increase in MLCK mRNA transcription and subsequent increase in MLCK protein expression and Caco-2 TJ permeability was mediated by activation of NF-κB. In conclusion, our data indicate that the IL-1β increase in Caco-2 TJ permeability was mediated by an increase in MLCK expression and activity. Our findings also indicate that the IL-1β-induced increase in MLCK protein expression and Caco-2 TJ permeability was mediated by an NF-κB-dependent increase in MLCK gene transcription.

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Section: Discussionmentioning

confidence: 99%

Mechanism of IL-1β-Induced Increase in Intestinal Epithelial Tight Junction Permeability

Al–Sadi

Dokładny

et al. 2008

The Journal of Immunology

371

295

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“…, where is the ratio of permeability of the monolayer to Na ϩ over the permeability to Cl Ϫ ( ϭ P Na / P Cl ), ⑀ is the dilution factor (⑀ ϭ C basal / C apical ), and v ϭ eV / kT (where V is the dilution potential, k is the Boltzmann constant, e is the elementary charge, and T is the Kelvin temperature) (19,20).…”

Section: Methodsmentioning

confidence: 99%

Autophagy Enhances Intestinal Epithelial Tight Junction Barrier Function by Targeting Claudin-2 Protein Degradation

Nighot

Thomas

2015

Journal of Biological Chemistry

198

158

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Background: How autophagy, a cell survival mechanism, regulates intestinal epithelial tight junction barrier or paracellular permeability is unknown. Results: Autophagy reduces the paracellular permeability of small solutes and ions via degradation of the pore-forming tight junction protein claudin-2. Conclusion: Autophagy enhances tight junction barrier function by targeting claudin-2. Significance: This is the first report showing autophagy regulation of the intestinal tight junction barrier.

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“…Cells with a number of passages ranging from 12 to 21 were grown for 12-20 days on Transwell or Snapwell membrane filters led to the establishment of TER values ranging from 1250 to 5000 ⍀.cm 2 . Such resistance variation is attributable to monolayer to monolayer variation in tight junction permeability (37).…”

Section: Transepithelial Resistance Measurementsmentioning

confidence: 99%

Polymeric IgA Is Superior to Monomeric IgA and IgG Carrying the Same Variable Domain in Preventing Clostridium difficile Toxin A Damaging of T84 Monolayers

Stubbe¹,

Berdoz²,

Kraehenbuhl³

et al. 2000

The Journal of Immunology

102

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The two exotoxins A and B produced by Clostridium difficile are responsible for antibiotic-associated enterocolitis in human and animals. When added apically to human colonic carcinoma-derived T84 cell monolayers, toxin A, but not toxin B, abolished the transepithelial electrical resistance and altered the morphological integrity. Apical addition of suboptimal concentration of toxin A made the cell monolayer sensitive to toxin B. Both toxins induced drastic and rapid epithelial alterations when applied basolaterally with a complete disorganization of tight junctions and vacuolization of the cells. Toxin A-specific IgG2a from hybridoma PCG-4 added apically with toxin A alone or in combination with toxin B abolished the toxin-induced epithelial alterations for up to 8 h. The Ab neutralized basolateral toxin A for 4 h, but not the mixture of the two toxins. Using an identical Ab:Ag ratio, we found that recombinant polymeric IgA (IgAd/p) with the same Fv fragments extended protection against toxin A for at least 24 h in both compartments. In contrast, the recombinant monomeric IgA counterpart behaved as the PCG-4 IgG2a Ab. The direct comparison between different Ig isotype and molecular forms, but of unique specificity, demonstrates that IgAd/p Ab is more efficient in neutralizing toxin A than monomeric IgG and IgA. We conclude that immune protection against C. difficile toxins requires toxin A-specific secretory Abs in the intestinal lumen and IgAd/p specific for both toxins in the lamina propria.

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Functional coupling of tight junctions and microfilaments in T84 monolayers

Cited by 98 publications

References 0 publications

Mechanism of IL-1β-Induced Increase in Intestinal Epithelial Tight Junction Permeability

Mechanism of IL-1β-Induced Increase in Intestinal Epithelial Tight Junction Permeability

Autophagy Enhances Intestinal Epithelial Tight Junction Barrier Function by Targeting Claudin-2 Protein Degradation

Polymeric IgA Is Superior to Monomeric IgA and IgG Carrying the Same Variable Domain in Preventing Clostridium difficile Toxin A Damaging of T84 Monolayers

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