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dc.contributor.author
Fischbarg, Jorge  
dc.date.available
2019-01-08T21:08:33Z  
dc.date.issued
2010-10  
dc.identifier.citation
Fischbarg, Jorge; Fluid transport across leaky epithelia: Central role of the tight junction and supporting role of aquaporins; American Physiological Society; Physiological Reviews; 90; 4; 10-2010; 1271-1290  
dc.identifier.issn
0031-9333  
dc.identifier.uri
http://hdl.handle.net/11336/67734  
dc.description.abstract
The mechanism of epithelial fluid transport remains unsolved, which is partly due to inherent experimental difficulties. However, a preparation with which our laboratory works, the corneal endothelium, is a simple leaky secretory epithelium in which we have made some experimental and theoretical headway. As we have reported, transendothelial fluid movements can be generated by electrical currents as long as there is tight junction integrity. The direction of the fluid movement can be reversed by current reversal or by changing junctional electrical charges by polylysine. Residual endothelial fluid transport persists even when no anions (hence no salt) are being transported by the tissue and is only eliminated when all local recirculating electrical currents are. Aquaporin (AQP) 1 is the only AQP present in these cells, and its deletion in AQP1 null mice significantly affects cell osmotic permeability (by ∼40%) but fluid transport much less (∼20%), which militates against the presence of sizable water movements across the cell. In contrast, AQP1 null mice cells have reduced regulatory volume decrease (only 60% of control), which suggests a possible involvement of AQP1 in either the function or the expression of volume-sensitive membrane channels/transporters. A mathematical model of corneal endothelium we have developed correctly predicts experimental results only when paracellular electro-osmosis is assumed rather than transcellular local osmosis. Our evidence therefore suggests that the fluid is transported across this layer via the paracellular route by a mechanism that we attribute to electro-osmotic coupling at the junctions. From our findings we have developed a novel paradigm for this preparation that includes 1) paracellular fluid flow; 2) a crucial role for the junctions; 3) hypotonicity of the primary secretion; and 4) an AQP role in regulation rather than as a significant water pathway. These elements are remarkably similar to those proposed by the laboratory of Adrian Hill for fluid transport across other leaky epithelia. Copyright © 2010 the American Physiological Society.  
dc.format
application/pdf  
dc.language.iso
eng  
dc.publisher
American Physiological Society  
dc.rights
info:eu-repo/semantics/openAccess  
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/  
dc.subject
Epithelia  
dc.subject
Transport  
dc.subject
Water  
dc.subject
Electroosmosis  
dc.subject.classification
Inmunología  
dc.subject.classification
Medicina Básica  
dc.subject.classification
CIENCIAS MÉDICAS Y DE LA SALUD  
dc.title
Fluid transport across leaky epithelia: Central role of the tight junction and supporting role of aquaporins  
dc.type
info:eu-repo/semantics/article  
dc.type
info:ar-repo/semantics/artículo  
dc.type
info:eu-repo/semantics/publishedVersion  
dc.date.updated
2019-01-07T13:32:12Z  
dc.journal.volume
90  
dc.journal.number
4  
dc.journal.pagination
1271-1290  
dc.journal.pais
Estados Unidos  
dc.journal.ciudad
Bethesda  
dc.description.fil
Fil: Fischbarg, Jorge. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Cardiológicas. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Investigaciones Cardiológicas; Argentina  
dc.journal.title
Physiological Reviews  
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/https://doi.org/10.1152/physrev.00025.2009  
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://www.physiology.org/doi/full/10.1152/physrev.00025.2009