The actin cytoskeleton in endothelial cell phenotypes

被引:220
作者
Prasain, Nutan [1 ,2 ]
Stevens, Troy [1 ,2 ]
机构
[1] Univ S Alabama, Coll Med, Ctr Lung Biol, Mobile, AL 36688 USA
[2] Univ S Alabama, Coll Med, Dept Mol & Cellular Pharmacol, Mobile, AL 36688 USA
关键词
Membrane skeleton; Stress fibers; Rho GTPases; Microtubules; cAMP; HEAT-SHOCK-PROTEIN; VASODILATOR-STIMULATED PHOSPHOPROTEIN; CA2+-INHIBITABLE ADENYLYL-CYCLASE; NUCLEOTIDE EXCHANGE FACTOR; LIGHT-CHAIN PHOSPHATASE; BARRIER FUNCTION; TIGHT JUNCTION; ALPHA-CATENIN; VE-CADHERIN; IN-VIVO;
D O I
10.1016/j.mvr.2008.09.012
中图分类号
R6 [外科学];
学科分类号
1002 ; 100210 ;
摘要
Endothelium forms a semi-permeable barrier that separates blood from the underlying tissue. Barrier function is largely determined by cell-cell and cell-matrix adhesions that define the limits of cell borders. Yet, such cell-cell and cell-matrix tethering is critically reliant upon the nature of adherence within the cell itself. Indeed, the actin cytoskeleton fulfills this essential function, to provide a strong, dynamic intracellular scaffold that organizes integral membrane proteins with the cell's interior, and responds to environmental cues to orchestrate appropriate cell shape. The actin cytoskeleton is comprised of three distinct but interrelated structures, including actin cross-linking of spectrin within the membrane skeleton, the cortical actin rim, and actomyosin-based stress fibers. This review addresses each of these actin-based structures, and discusses cellular signals that control the disposition of actin in different endothelial cell phenotypes. (C) 2008 Published by Elsevier Inc.
引用
收藏
页码:53 / 63
页数:11
相关论文
共 179 条
[1]   Endothelial cell heterogeneity [J].
Aird, WC .
CRITICAL CARE MEDICINE, 2003, 31 (04) :S221-S230
[2]  
Aird WC, 2008, PHARMACOL REP, V60, P139
[3]   Phenotypic heterogeneity of the endothelium I. Structure, function, and mechanisms [J].
Aird, William C. .
CIRCULATION RESEARCH, 2007, 100 (02) :158-173
[4]   Phenotypic heterogeneity of the endothelium II. Representative vascular beds [J].
Aird, William C. .
CIRCULATION RESEARCH, 2007, 100 (02) :174-190
[5]   Activation of RhoA by thrombin in endothelial hyperpermeability - Role of Rho kinase and protein tyrosine kinases [J].
Amerongen, GPV ;
van Delft, S ;
Vermeer, MA ;
Collard, JG ;
van Hinsbergh, VWM .
CIRCULATION RESEARCH, 2000, 87 (04) :335-340
[6]   Transient and prolonged increase in endothelial permeability induced by histamine and thrombin -: Role of protein kinases, calcium, and RhoA [J].
Amerongen, GPV ;
Draijer, R ;
Vermeer, MA ;
van Hinsbergh, VWM .
CIRCULATION RESEARCH, 1998, 83 (11) :1115-1123
[7]   Endothelial cell-to-cell junctions: Molecular organization and role in vascular homeostasis [J].
Bazzoni, G ;
Dejana, E .
PHYSIOLOGICAL REVIEWS, 2004, 84 (03) :869-901
[8]  
Bearer EL, 2000, CELL MOTIL CYTOSKEL, V47, P351, DOI 10.1002/1097-0169(200012)47:4<351::AID-CM8>3.0.CO
[9]  
2-8
[10]   Dimerization of the highly conserved light chain shared by dynein and myosin V [J].
Benashski, SE ;
Harrison, A ;
PatelKing, RS ;
King, SM .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1997, 272 (33) :20929-20935