Regulation of epithelial tight junction permeability by cyclic AMP

Duffey, Michael E.; Hainau, Bo; Ho, Shu Cheow; Bentzel, Carl J.

doi:10.1038/294451a0

Cited by 286 publications

(128 citation statements)

References 9 publications

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“…This paradigm was shattered when regulation of Necturus gallbladder epithelial tight junction permeability by cyclic adenosine monophosphate (AMP) was reported. 21 This study noted that changes in tight junction permeability were accompanied by reorganization of tight junction ultrastructure, suggesting a link between structural and functional regulation. 21 Despite this remarkable observation, the mechanisms of tight junction regulation remained unexplored.…”

Section: Tight Junctions Are Intimately Related To the Perijunctionalmentioning

confidence: 99%

“…21 This study noted that changes in tight junction permeability were accompanied by reorganization of tight junction ultrastructure, suggesting a link between structural and functional regulation. 21 Despite this remarkable observation, the mechanisms of tight junction regulation remained unexplored. One important clue to these mechanisms came from studies showing the association of thin actin-like filaments within the apical cytoplasm of small intestinal epithelia with tight junctions.…”

Section: Tight Junctions Are Intimately Related To the Perijunctionalmentioning

confidence: 99%

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Molecular Basis of Epithelial Barrier Regulation

Turner

2006

The American Journal of Pathology

488

166

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The intestinal epithelium is faced with the complex task of providing a barrier while also allowing nutrient and water absorption. The frequency with which these processes are disrupted in disease can be taken as evidence of their importance. It is therefore of interest to define the mechanisms of altered intestinal barrier and transport function and develop means to correct diseaseassociated defects. Over the past 10 years, some of the molecular events underlying physiological epithelial barrier regulation have been described. Remarkably, recent advances have shown that activation of the same mechanisms is central to barrier dysfunction in both in vitro and in vivo models of disease. Although the contribution of barrier dysfunction to pathogenesis of chronic disease remains incompletely understood, it is now clear that cytoskeletal regulation of barrier function is both an important pathogenic process and that targeted inhibition of myosin light chain kinase, which affects this cytoskeleton-dependent tight junction dysfunction, is an attractive candidate for therapeutic intervention.

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Section: Tight Junctions Are Intimately Related To the Perijunctionalmentioning

confidence: 99%

Section: Tight Junctions Are Intimately Related To the Perijunctionalmentioning

confidence: 99%

Molecular Basis of Epithelial Barrier Regulation

Turner

2006

The American Journal of Pathology

488

166

View full text Add to dashboard Cite

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“…These so called dilution potentials are indicators for the ion selectivity of the epithelium and changes in these transepithelial potential differences reflect changes in ion selectivity of the paracellular pathway if the ion permeability of the cell membranes remains unaltered. The conclusion that the ion selectivity of tight junctions of Necturus gallbladder [11] can be modulated by cAMP must be questioned since (i) it is known now that in this tissue cAMP also induces an increase of the Cl − conductance in the apical cell membranes [26], thereby reducing the cation selectivity of the tissue, (ii) cAMP induced a decrease of the transepithelial conductance in the gallbladder due to a collapse of the lateral intercellular space [19]. This makes this part of the paracellular pathway more important and because the transport numbers (t) in the lateral intercellular spaces are based on free solution mobility, with t Cl > t Na , the cation selectivity of the paracellular pathway should decrease.…”

Section: Introductionmentioning

confidence: 99%

“…This is because the paracellular pathway dominates the transepithelial permeability and the tight junctions have a larger conductance for cations. It has been reported that the cation selectivity of these epithelia can be decreased by cAMPgenerating drugs [4,11,27]. This conclusion is primarily based on measurements of diffusion potentials induced by replacing part of the NaCl in the bathing solution at one side of the epithelium by an inert nonelectrolyte.…”

Section: Introductionmentioning

confidence: 99%

“…Bumetanide causes a strong reduction of the forskolin-evoked potential change in rat ileum [16]. The Cl − permeability at the basolateral side of the epithelial cells is not affected by forskolin [11] and, in the presence of a K + -channel blocker in the serosal bath, application of forskolin will not change the cellular component of the ion selectivity at the basolateral side.…”

Section: Introductionmentioning

confidence: 99%

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The Chloride Conductance of Tight Junctions of Rat Ileum Can Be Increased by cAMP But Not by Carbachol

Bijlsma

Bakker

Groot

1997

Journal of Membrane Biology

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The chloride conductance of tight junctions of rat ileum can be increased by cAMP but not by carbachol Bijlsma, P.B.; Bakker, R.C. Published in:The journal of membrane biology DOI:10.1007/s002329900222Link to publication Citation for published version (APA):Bijlsma, P. B., & Bakker, R. C. (1997). The chloride conductance of tight junctions of rat ileum can be increased by cAMP but not by carbachol. The journal of membrane biology, 157(2), 127-137. DOI: 10.1007/s002329900222 General rightsIt is not permitted to download or to forward/distribute the text or part of it without the consent of the author(s) and/or copyright holder(s), other than for strictly personal, individual use, unless the work is under an open content license (like Creative Commons). Disclaimer/Complaints regulationsIf you believe that digital publication of certain material infringes any of your rights or (privacy) interests, please let the Library know, stating your reasons. In case of a legitimate complaint, the Library will make the material inaccessible and/or remove it from the website. Please Ask the Library: http://uba.uva.nl/en/contact, or a letter to: Library of the University of Amsterdam, Secretariat, Singel 425, 1012 WP Amsterdam, The Netherlands. You will be contacted as soon as possible. Abstract. It is well known, that in mammalian small intestine, cAMP increases Cl − permeability of the apical membrane of enterocytes as part of its secretory action. Paradoxically, this is usually accompanied by an increase of the transepithelial resistance. In the present study we report that in the presence of bumetanide (to block basolateral Cl − uptake) cAMP always decreased the transepithelial resistance. We examined whether this decrease in resistance was due to a cAMP-dependent increase of the paracellular electrolyte permeability in addition to the increase of the Cl − permeability of the apical cell membrane. We used diffusion potentials induced by serosal replacement of NaCl, and transepithelial current passage to evoke transport number effects. The results revealed that cAMP (but not carbachol) could increase the Cl − permeability of the tight junctions in rat ileum. Moreover, we observed a variation in transepithelial resistance of individual tissue preparations, inversely related to the cation selectivity of the tissue, suggesting that Na + permeability of the tight junctions can vary between preparations.

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Epithelial permeability induced by neutrophil transmigration is potentiated by hypoxia: Role of intracellular cAMP

Friedman¹,

Taylor²,

Parkos

et al. 1998

J. Cell. Physiol.

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Mucosal tissues, such as the lung and intestine, are primary targets for ischemic damage. Under these conditions, neutrophil (polymorphonuclear leukocyte; PMN) infiltration into the protective epithelium has been implicated as a pathophysiologic mediator. Because PMN transepithelial migration results in increased paracellular permeability, and because our previous data revealed that epithelial hypoxia enhances PMN transmigration, we hypothesized that macromolecular permeability may be altered in epithelium exposed to hypoxia and reoxygenation (H/R) in the presence of PMNs. Human intestinal epithelia (T84) were grown on permeable supports, exposed to cellular hypoxia (pO2 20 torr) for 0-72 hr, and examined for increases in PMN-evoked permeability by using standard flux assays. Increasing epithelial hypoxia potentiated PMN-induced permeability of labeled paracellular tracers (size range 3-500 kD). Such increases were blocked by monoclonal antibody (mAb) to the PMN integrin CD11b (82 +/- 1% decreased compared with control mAb) and were partially blocked by anti-CD47 mAb (51 +/- 1%). Assessment of barrier recovery revealed that monolayers exposed to H/R were significantly diminished in their ability to reseal following PMN transmigration (recovery of 36 +/- 6% in H/R vs. 94 +/- 2% in normoxic controls). Because intracellular cyclic AMP (cAMP) has been demonstrated to regulate epithelial permeability, and because PMN-derived compound(s), (i.e., 5'-adenosine monophosphate; AMP) elevate epithelial cAMP, we examined the impact of hypoxia on epithelial cAMP responses. These experiments revealed that hypoxic epithelia were diminished in their ability to generate cAMP, and pharmacologic elevation (8-bromo-cAMP) of intracellular cAMP in hypoxic cells normalized both PMN-induced permeability changes and restoration of barrier function. These results support a role for PMN in increased intestinal permeability associated with reperfusion injury and imply a substantial role for cAMP signaling in maintenance of permeability during PMN transmigration.

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Regulation of epithelial tight junction permeability by cyclic AMP

Cited by 286 publications

References 9 publications

Molecular Basis of Epithelial Barrier Regulation

Molecular Basis of Epithelial Barrier Regulation

The Chloride Conductance of Tight Junctions of Rat Ileum Can Be Increased by cAMP But Not by Carbachol

Epithelial permeability induced by neutrophil transmigration is potentiated by hypoxia: Role of intracellular cAMP

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