Document Detail

A transmural pressure gradient induces mechanical and biological adaptive responses in endothelial cells.
MedLine Citation:
PMID:  14527936     Owner:  NLM     Status:  MEDLINE    
A sudden increase in the transmural pressure gradient across endothelial monolayers reduces hydraulic conductivity (L(p)), a phenomenon known as the sealing effect. To further characterize this endothelial adaptive response, we measured bovine aortic endothelial cell (BAEC) permeability to albumin and 70-kDa dextran, L(p), and the solvent-drag reflection coefficients (sigma) during the sealing process. The diffusional permeability coefficients for albumin (1.33 +/- 0.18 x 10(-6) cm/s) and dextran (0.60 +/- 0.16 x 10(-6) cm/s) were measured before pressure application. The effective permeabilities (measured when solvent drag contributes to solute transport) of albumin and dextran (P(ealb) and P(edex)) were measured after the application of a 10 cmH(2)O pressure gradient; during the first 2 h of pressure application, P(ealb), P(edex), and L(p) were significantly reduced by 2.0 +/- 0.3-, 2.1 +/- 0.3-, and 3.7 +/- 0.3-fold, respectively. Immunostaining of the tight junction (TJ) protein zonula occludens-1 (ZO-1) was significantly increased at cell-cell contacts after the application of transmural pressure. Cytochalasin D treatment significantly elevated transport but did not inhibit the adaptive response, whereas colchicine treatment had no effect on diffusive permeability but inhibited the adaptive response. Neither cytoskeletal inhibitor altered sigma despite significantly elevating both L(p) and effective permeability. Our data suggest that BAECs actively adapt to elevated transmural pressure by mobilizing ZO-1 to intercellular junctions via microtubules. A mechanical (passive) component of the sealing effect appears to reduce the size of a small pore system that allows the transport of water but not dextran or albumin. Furthermore, the structures of the TJ determine transport rates but do not define the selectivity of the monolayer to solutes (sigma).
Lucas DeMaio; John M Tarbell; Russell C Scaduto; Thomas W Gardner; David A Antonetti
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.     Date:  2003-10-02
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  286     ISSN:  0363-6135     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2004 Feb 
Date Detail:
Created Date:  2004-01-12     Completed Date:  2004-03-09     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H731-41     Citation Subset:  IM    
Department of Chemical Engineering, Biomolecular Transport Dynamics Laboratory, The Pennsylvania State University, University Park 16802, USA.
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MeSH Terms
Aorta / physiology
Biological Transport / drug effects
Cell Membrane / physiology
Cell Membrane Permeability / drug effects,  physiology*
Cells, Cultured
Colchicine / pharmacology
Cytochalasin D / pharmacology
Dextrans / metabolism
Endothelium, Vascular / physiology*
Membrane Proteins / drug effects,  physiology
Phosphoproteins / drug effects,  physiology
Serum Albumin / metabolism
Grant Support
Reg. No./Substance:
0/Membrane Proteins; 0/Phosphoproteins; 0/Serum Albumin; 0/zonula occludens-1 protein; 22144-77-0/Cytochalasin D; 64-86-8/Colchicine; 9004-54-0/Dextrans

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