Na,K-ATPase inhibition alters tight junction structure  and permeability in human retinal pigment epithelial cells

Rajasekaran, Sigrid A.; Hu, Jane; Gopal, Jegan; Gallemore, Ron P.; Ryazantsev, Sergey; Bok, Dean; Rajasekaran, Ayyappan K.

doi:10.1152/ajpcell.00355.2002

Cited by 106 publications

(80 citation statements)

References 51 publications

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“…Additionally, chronic Mn exposure might alter systematic homeostasis of calcium, leading to a further impairment of Na ϩ ,K ϩ -ATPase function (14,50). As a further barrier integrity disturbing mechanism, occludin immunocytochemistry studies reveal a disturbance of tight junction structure, which might also be partly caused by an inhibition of Na ϩ ,K ϩ -ATPase function (51).…”

Section: Discussionmentioning

confidence: 99%

Impact of Manganese on and Transfer across Blood-Brain and Blood-Cerebrospinal Fluid Barrier in Vitro

Bornhorst

Wehe

Hüwel

et al. 2012

Journal of Biological Chemistry

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Background: Modes of neurotoxic action after Mn overexposure are not fully understood. Results:The blood-CSF barrier showed higher Mn sensitivity and active Mn transport properties. Conclusion:The blood-CSF barrier might be the major route for Mn into the brain. Significance: Deeper insight in the impact of Mn on and its transfer across brain barrier systems might help to prevent irreversible neurological damage.

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Section: Discussionmentioning

confidence: 99%

Impact of Manganese on and Transfer across Blood-Brain and Blood-Cerebrospinal Fluid Barrier in Vitro

Bornhorst

Wehe

Hüwel

et al. 2012

Journal of Biological Chemistry

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“…The Na + /K + ATPase is required for tight junction formation, but in most epithelia is localized to the basolateral membrane, separate from the apical tight junction (Rajasekaran et al, 2001;Violette et al, 2006). An exception are the retinal pigment epithelial cells, where the Na + /K + ATPase is apically localized and required for tight junction structure and function (Rajasekaran et al, 2003).…”

Section: The Septate Junction and Its Originsmentioning

confidence: 99%

Making the connection – shared molecular machinery and evolutionary links underlie the formation and plasticity of occluding junctions and synapses

Harden

Wang

Krieger

2016

Journal of Cell Science

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The pleated septate junction ( pSJ), an ancient structure for cell-cell contact in invertebrate epithelia, has protein components that are found in three more-recent junctional structures, the neuronal synapse, the paranodal region of the myelinated axon and the vertebrate epithelial tight junction. These more-recent structures appear to have evolved through alterations of the ancestral septate junction. During its formation in the developing animal, the pSJ exhibits plasticity, although the final structure is extremely robust. Similar to the immature pSJ, the synapse and tight junctions both exhibit plasticity, and we consider evidence that this plasticity comes at least in part from the interaction of members of the immunoglobulin cell adhesion molecule superfamily with highly regulated membraneassociated guanylate kinases. This plasticity regulation probably arose in order to modulate the ancestral pSJ and is maintained in the derived structures; we suggest that it would be beneficial when studying plasticity of one of these structures to consider the literature on the others. Finally, looking beyond the junctions, we highlight parallels between epithelial and synaptic membranes, which both show a polarized distribution of many of the same proteins -evidence that determinants of apicobasal polarity in epithelia also participate in patterning of the synapse.

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“…While in the second group of cells, the Na + -K + -ATPase is located in the serosal side, which could be involved in recycling K + and possibly other unknown function. Intriguingly, Na + -K + -ATPase has also been discovered on the apical membrane in other epithelial cells, for example, in the chordoid plexus [29,30] and retinal pigment epithelium [31,32]. These mechanisms are probably involved in maintaining an adequate volume and physiological composition of the pleural fluid and of mesothelial cell cytoplasm [20,21].…”

Section: I-2 Na + -K + -Atpase and Ca 2+ -Atpasementioning

confidence: 99%

Electrolyte and Fluid Transport in Mesothelial Cells

Ji¹,

Nie²

2008

JEBP

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Mesothelial cells are specialized epithelial cells, which line the pleural, pericardial, and peritoneal cavities. Accumulating evidence suggests that the monolayer of mesothelial cells is permeable to electrolyte and fluid, and thereby govern both fluid secretion and re-absorption in the serosal cavities. Disorders in these salt and fluid transport systems may be fundamental in the pathogenesis of pleural effusion, pericardial effusion, and ascites. In this review, we discuss the location, physiological function, and regulation of active transport (Na + -K + -ATPase) systems, cation and anion channels (Na + , K + , Cl − , and Ca 2+ channels), antiport (exchangers) systems, and symport (co-transporters) systems, and water channels (aquaporins). These secretive and absorptive pathways across mesothelial monolayer cells for electrolytes and fluid may provide pivotal therapeutical targets for novel clinical intervention in edematous diseases of serous cavities. Keywords mesothelioma; ion channel; permeability; effusion; filtration; ENaC Mesothelial cells are specialized epithelial cells that line the serous cavities, including the pleural, pericardial, and peritoneal cavities in addition to internal organs [1]. While the mesothelium was first described more than a century ago, one of its critical essential functions, namely, its active roles in transerosal transport, in particular, cavity fluid secretion and reabsorption, was long overlooked. Only in last two decades compelling evidence accumulated that mesothelial cells actively transport electrolytes and fluid and, in turn, regulate liquid volume within the cavities. The mesothelium, on the basis of recent increasing experimental evidence, both in vitro and in vivo, is less permeable to electrolytes than was previously assumed, with ion permeability characteristics similar to those in epithelia [2,3]. Herein this article we will review the expression and biophysical features of salt and fluid transport systems, both active and passive, that have been identified in mesothelial cells (Fig. 1, Tables 1 and 2). I. ION CHANNELS AND ATPASE I-1. Amiloride-Inhibitable Cation ChannelsThe epithelial sodium channel (ENaC), as a major pathway which participates in sodium movement across the apical membrane of polarized epithelial cells, has been cloned and characterized [4][5][6] ENaC subunits have been cloned to date, namely α-, β-, γ-, δ-, and ε-ENaC [7]. The biophysical properties of various ENaC channels depend on their subunit compositions. When expressed in oocytes one of "conductive" subunits (α, δ, and ε-ENaC) can form a channel sharing identical biophysical properties to three-subunit channels composed of both a "conductive" subunit and two "non-conductive" subunits, namely, β-and γ-ENaCs. When α-, β-, and γ-ENaC subunits are assembled together, the result is a 4-to 6-pS channel that is highly selective for Na + over K + . In contrast, two-subunit α β-and α γ-ENaC channels display diverse amiloride sensitivity, conductance, and Na + permeability [8]. ENaC is...

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Na,K-ATPase inhibition alters tight junction structure and permeability in human retinal pigment epithelial cells

Cited by 106 publications

References 51 publications

Impact of Manganese on and Transfer across Blood-Brain and Blood-Cerebrospinal Fluid Barrier in Vitro

Impact of Manganese on and Transfer across Blood-Brain and Blood-Cerebrospinal Fluid Barrier in Vitro

Making the connection – shared molecular machinery and evolutionary links underlie the formation and plasticity of occluding junctions and synapses

Electrolyte and Fluid Transport in Mesothelial Cells

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