Endothelial cell barrier regulation by sphingosine 1-phosphate

Bryan J. McVerry, Joe GN Garcia

Research output: Contribution to journalArticle

144 Citations (Scopus)

Abstract

Disruption of vascular barrier integrity markedly increases permeability to fluid and solute and is the central pathophysiologic mechanism of many inflammatory disease processes, including sepsis and acute lung injury (ALI). Dynamic control of the endothelial barrier involves complex signaling to the endothelial cytoskeleton and to adhesion complexes between neighboring cells and between cells and the underlying matrix. Sphingosine 1-phosphate (S1P), a biologically active lipid generated by hydrolysis of membrane lipids in activated platelets, organizes actin into a strong cortical ring and strengthens both intercellular and cell-matrix adherence. The mechanisms by which S1P increases endothelial barrier integrity remain the focus of intense basic research. The downstream structural changes induced by S1P interact to decrease vascular permeability to fluid and solute, which translates into a reduction lung edema formation in animal models of ALI, thus suggesting a potentially life-saving therapeutic role for vascular barrier modulation in critically ill patients.

Original languageEnglish (US)
Pages (from-to)1075-1085
Number of pages11
JournalJournal of Cellular Biochemistry
Volume92
Issue number6
DOIs
StatePublished - 2004
Externally publishedYes

Fingerprint

Endothelial cells
Endothelial Cells
Acute Lung Injury
Blood Vessels
Fluids
Capillary Permeability
Membrane Lipids
Platelets
Cytoskeleton
Critical Illness
Actins
Hydrolysis
Permeability
Edema
Sepsis
Animals
Blood Platelets
Adhesion
Animal Models
Modulation

Keywords

  • Cadherin
  • Cytoskeleton
  • Endothelial permeability
  • Rac GTPase
  • Rho GTPase

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology

Cite this

Endothelial cell barrier regulation by sphingosine 1-phosphate. / McVerry, Bryan J.; Garcia, Joe GN.

In: Journal of Cellular Biochemistry, Vol. 92, No. 6, 2004, p. 1075-1085.

Research output: Contribution to journalArticle

@article{c34f004475644a328826ac5e1fdcad17,
title = "Endothelial cell barrier regulation by sphingosine 1-phosphate",
abstract = "Disruption of vascular barrier integrity markedly increases permeability to fluid and solute and is the central pathophysiologic mechanism of many inflammatory disease processes, including sepsis and acute lung injury (ALI). Dynamic control of the endothelial barrier involves complex signaling to the endothelial cytoskeleton and to adhesion complexes between neighboring cells and between cells and the underlying matrix. Sphingosine 1-phosphate (S1P), a biologically active lipid generated by hydrolysis of membrane lipids in activated platelets, organizes actin into a strong cortical ring and strengthens both intercellular and cell-matrix adherence. The mechanisms by which S1P increases endothelial barrier integrity remain the focus of intense basic research. The downstream structural changes induced by S1P interact to decrease vascular permeability to fluid and solute, which translates into a reduction lung edema formation in animal models of ALI, thus suggesting a potentially life-saving therapeutic role for vascular barrier modulation in critically ill patients.",
keywords = "Cadherin, Cytoskeleton, Endothelial permeability, Rac GTPase, Rho GTPase",
author = "McVerry, {Bryan J.} and Garcia, {Joe GN}",
year = "2004",
doi = "10.1002/jcb.20088",
language = "English (US)",
volume = "92",
pages = "1075--1085",
journal = "Journal of Cellular Biochemistry",
issn = "0730-2312",
publisher = "Wiley-Liss Inc.",
number = "6",

}

TY - JOUR

T1 - Endothelial cell barrier regulation by sphingosine 1-phosphate

AU - McVerry, Bryan J.

AU - Garcia, Joe GN

PY - 2004

Y1 - 2004

N2 - Disruption of vascular barrier integrity markedly increases permeability to fluid and solute and is the central pathophysiologic mechanism of many inflammatory disease processes, including sepsis and acute lung injury (ALI). Dynamic control of the endothelial barrier involves complex signaling to the endothelial cytoskeleton and to adhesion complexes between neighboring cells and between cells and the underlying matrix. Sphingosine 1-phosphate (S1P), a biologically active lipid generated by hydrolysis of membrane lipids in activated platelets, organizes actin into a strong cortical ring and strengthens both intercellular and cell-matrix adherence. The mechanisms by which S1P increases endothelial barrier integrity remain the focus of intense basic research. The downstream structural changes induced by S1P interact to decrease vascular permeability to fluid and solute, which translates into a reduction lung edema formation in animal models of ALI, thus suggesting a potentially life-saving therapeutic role for vascular barrier modulation in critically ill patients.

AB - Disruption of vascular barrier integrity markedly increases permeability to fluid and solute and is the central pathophysiologic mechanism of many inflammatory disease processes, including sepsis and acute lung injury (ALI). Dynamic control of the endothelial barrier involves complex signaling to the endothelial cytoskeleton and to adhesion complexes between neighboring cells and between cells and the underlying matrix. Sphingosine 1-phosphate (S1P), a biologically active lipid generated by hydrolysis of membrane lipids in activated platelets, organizes actin into a strong cortical ring and strengthens both intercellular and cell-matrix adherence. The mechanisms by which S1P increases endothelial barrier integrity remain the focus of intense basic research. The downstream structural changes induced by S1P interact to decrease vascular permeability to fluid and solute, which translates into a reduction lung edema formation in animal models of ALI, thus suggesting a potentially life-saving therapeutic role for vascular barrier modulation in critically ill patients.

KW - Cadherin

KW - Cytoskeleton

KW - Endothelial permeability

KW - Rac GTPase

KW - Rho GTPase

UR - http://www.scopus.com/inward/record.url?scp=16644394172&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=16644394172&partnerID=8YFLogxK

U2 - 10.1002/jcb.20088

DO - 10.1002/jcb.20088

M3 - Article

C2 - 15258893

AN - SCOPUS:16644394172

VL - 92

SP - 1075

EP - 1085

JO - Journal of Cellular Biochemistry

JF - Journal of Cellular Biochemistry

SN - 0730-2312

IS - 6

ER -