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Titolo:
Cytoskeletal regulation of pulmonary vascular permeability
Autore:
Dudek, SM; Garcia, JGN;
Indirizzi:
Johns Hopkins Univ, Sch Med, Johns Hopkins Asthma & Allergy Ctr, Div Pulm & Crit Care Med, Baltimore, MD 21224 USA Johns Hopkins Univ Baltimore MD USA 21224 re Med, Baltimore, MD 21224 USA
Titolo Testata:
JOURNAL OF APPLIED PHYSIOLOGY
fascicolo: 4, volume: 91, anno: 2001,
pagine: 1487 - 1500
SICI:
8750-7587(200110)91:4<1487:CROPVP>2.0.ZU;2-3
Fonte:
ISI
Lingua:
ENG
Soggetto:
LIGHT-CHAIN KINASE; HUMAN ENDOTHELIAL-CELLS; INDUCED LUNG INJURY; ACTIN STRESS FIBERS; ADHERENS JUNCTION PROTEINS; MONOLAYER BARRIER FUNCTION; CADHERIN-CATENIN COMPLEX; CYTOSOLIC FREE CALCIUM; ISOLATED RAT LUNGS; SHEAR-STRESS;
Keywords:
cytoskeleton; endothelium; actomyosin contraction; actin-binding proteins; acute lung injury;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
163
Recensione:
Indirizzi per estratti:
Indirizzo: Garcia, JGN Johns Hopkins Univ, Sch Med, Johns Hopkins Asthma & Allergy Ctr, Div Pulm & Crit Care Med, 5501 Hopkins Bayview Circle, Baltimore, MD 21224 USA Johns Hopkins Univ 5501 Hopkins Bayview Circle Baltimore MD USA 21224
Citazione:
S.M. Dudek e J.G.N. Garcia, "Cytoskeletal regulation of pulmonary vascular permeability", J APP PHYSL, 91(4), 2001, pp. 1487-1500

Abstract

The endothelial cell (EC) lining of the pulmonary vasculature forms a semipermeable barrier between the blood and the interstitium of the lung. Disruption of this barrier occurs during inflammatory disease states such as acute lung injury and acute respiratory distress syndrome and results in the movement of fluid and macromolecules into the interstitium. and pulmonary air spaces. These processes significantly contribute to the high morbidity and mortality of patients afflicted with acute lung injury. The critical importance of pulmonary vascular barrier function is shown by the balance between competing EC contractile forces, which generate centripetal tension, andadhesive cell-cell and cell-matrix tethering forces, which regulate cell shape. Both competing forces in this model are intimately linked through theendothelial cytoskeleton, a complex network of actin microfilaments, microtubules, and intermediate filaments, which combine to regulate shape changeand transduce signals within and between EC. A key EC contractile event inseveral models of agonist-induced barrier dysfunction is the phosphorylation of regulatory myosin light chains catalyzed by Ca2+/calmodulin-dependentmyosin light chain kinase and/or through the activity of the Rho/Rho kinase pathway. Intercellular contacts along the endothelial monolayer consist primarily of two types of complexes (adherens junctions and tight junctions), which link to the actin cytoskeleton to provide both mechanical stabilityand transduction of extracellular signals into the cell. Focal adhesions provide additional adhesive forces in barrier regulation by forming a critical bridge for bidirectional signal transduction between the actin cytoskeleton and the cell-matrix interface. Increasingly, the effects of mechanical forces such as shear stress and ventilator-induced stretch on EC barrier function are being recognized. The critical role of the endothelial cytoskeleton in integrating these multiple aspects of pulmonary vascular permeability provides a fertile area for the development of clinically important barrier-modulating therapies.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 06/04/20 alle ore 04:49:57