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Titolo:
Differential regulation of sphingosine-1-phosphate and VEGF-induced endothelial cell chemotaxis - Involvement of G(i alpha 2)-linked rho kinase activity
Autore:
Liu, F; Verin, AD; Wang, P; Day, R; Wersto, RP; Chrest, FJ; English, DK; Garcia, JGN;
Indirizzi:
Johns Hopkins Univ, Sch Med, Div Pulm & Crit Care Med, Baltimore, MD 21205USA Johns Hopkins Univ Baltimore MD USA 21205 are Med, Baltimore, MD 21205USA NIA, Baltimore, MD 21224 USA NIA Baltimore MD USA 21224NIA, Baltimore, MD 21224 USA Methodist Res Inst, Indianapolis, IN USA Methodist Res Inst Indianapolis IN USA st Res Inst, Indianapolis, IN USA Tufts Univ, Boston, MA 02111 USA Tufts Univ Boston MA USA 02111Tufts Univ, Boston, MA 02111 USA
Titolo Testata:
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY
fascicolo: 6, volume: 24, anno: 2001,
pagine: 711 - 719
SICI:
1044-1549(200106)24:6<711:DROSAV>2.0.ZU;2-Y
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROTEIN-COUPLED RECEPTORS; FOCAL ADHESION KINASE; MYOSIN LIGHT-CHAIN; SPHINGOSINE 1-PHOSPHATE; LYSOPHOSPHATIDIC ACID; GROWTH-FACTOR; ACTIN REORGANIZATION; SIGNAL-TRANSDUCTION; PHARMACOLOGICAL PROPERTIES; MEDIATED PHOSPHORYLATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
51
Recensione:
Indirizzi per estratti:
Indirizzo: Garcia, JGN Johns Hopkins Asthma & Allergy Ctr, 5501 Hopkins Bayview Circle,4B-77, Baltimore, MD 21224 USA Johns Hopkins Asthma & Allergy Ctr 5501 Hopkins Bayview Circle,4B-77 Baltimore MD USA 21224
Citazione:
F. Liu et al., "Differential regulation of sphingosine-1-phosphate and VEGF-induced endothelial cell chemotaxis - Involvement of G(i alpha 2)-linked rho kinase activity", AM J RESP C, 24(6), 2001, pp. 711-719

Abstract

We compared stimulus-coupling pathways involved in bovine pulmonary artery(PA) and lung microvascular endothelial cell migration evoked by sphingosine-l-phosphate (S1P), a potent bioactive lipid released from activated platelets, and by vascular endothelial growth factor (VEGF), a well-recognized angiogenic factor. S1P-induced endothelial cell migration was maximum at 1 muM (similar to 8-fold increase with PA endothelium) and surpassed the maximal response evoked by either VEGF (10 ng/ml) (similar to 2.5-fold increase) or hepatocyte growth factor (HGF) (similar to 2.5-foId increase). Migration induced by S1P, but not by VEGF, was significantly inhibited by treatment with antisense oligonucleotides directed to Edg-1 and Edg-3 (endothelial differentiation gene) S1P receptors and by G protein modification. These strategies included pretreatment with pertussis toxin, or transfection with mini-genes encoding a py subunit inhibitory peptide of the beta -adrenergic receptor kinase, or an 11-amino-acid peptide that inhibits G(1 alpha2) signaling. Various strategies to interrupt Rho family signaling, including C-3 exotoxin, dominant/negative Rho, or the addition of Y27632, a cell-permeable Rho kinase inhibitor, significantly attenuated S1P- but not VEGF-induced migration. Conversely, pharmacologic Inhibition of either myosin light chain kinase, src family tyrosine kinases, or phosphatidylinositol-3' kinase reduced basal endothelial cell migration and abolished VEGF-induced endothelial cell migration but did not inhibit the increase in S1P-induced migration. Whereas VEGF and S1P increased both p42/p44 extracellular regulated kinase and p38 mitogen-activated protein (MAP) kinase activities, only p38 MAP kinase inhibition significantly reduced VEGF- and S1P-stimulated migration. These data confirm S1P as a potent endothelial cell chemoattractant throughG(1 alpha2)-coupled Edg receptors linked to Rho-associated kinase and p38 MAP kinase activation. The divergence in signaling pathways evoked by S1P and VEGF suggests complex and agonist-specific regulation of endothelial cell angiogenic responses.

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Documento generato il 25/11/20 alle ore 18:04:45