Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1 Pt 1
pubmed:dateCreated
1998-2-19
pubmed:abstractText
Previously, we demonstrated the role of nitric oxide (NO) in transforming epithelial cells from a stationary to locomoting phenotype [E. Noiri, T. Peresleni, N. Srivastava, P. Weber, W.F. Bahou, N. Peunova, and M. S. Goligorsky. Am. J. Physiol. 270 (Cell Physiol. 39): C794-C802, 1996] and its permissive function in endothelin-1-stimulated endothelial cell migration (E. Noiri, Y. Hu, W. F. Bahou; C. Keese, I. Giaever, and M. S. Goligorsky, J. Biol: Chem. 272: 1747-1753, 1997). In the present study, the role of functional NO synthase in executing the vascular endothelial growth factor (VEGF)-guided program of endothelial cell migration and angiogenesis was studied in two independent experimental settings. First, VEGF, shown to stimulate NO release from simian virus 40-immortalized microvascular endothelial cells, induced endothelial cell transwell migration, whereas NG-nitro-L-arginine methyl ester (L-NAME) or antisense oligonucleotides to endothelial NO synthase suppressed this effect of VEGF. Second, in a series of experiments on endothelial cell wound healing, the rate of VEGF-stimulated cell migration was significantly blunted by the inhibition of NO synthesis. To gain insight into the possible mode of NO action, we next addressed the possibility that NO modulates cell matrix adhesion by performing impedance analysis of endothelial cell monolayers subjected to NO. The data showed the presence of spontaneous fluctuations of the resistance in ostensibly stationary endothelial cells. Spontaneous oscillations were induced by NO, which also inhibited cell matrix adhesion. This process we propose to term "podokinesis" to emphasize a scalar from of micromotion that, in the presence of guidance cues, e.g., VEGF, is transformed to a vectorial movement. In conclusion, execution of the program for directional endothelial cell migration requires two coexisting messages: NO-induced podokinesis (scalar motion) and guidance cues, e.g., VEGF, which imparts a vectorial component to the movement. Such a requirement for the dual signaling may explain a mismatch in the demand and supply with newly formed vessels in different pathological states accompanied by the inhibition of NO synthase.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
274
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
C236-44
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:9458733-Animals, pubmed-meshheading:9458733-Cell Adhesion, pubmed-meshheading:9458733-Cell Movement, pubmed-meshheading:9458733-Cells, Cultured, pubmed-meshheading:9458733-Endothelial Growth Factors, pubmed-meshheading:9458733-Endothelium, Vascular, pubmed-meshheading:9458733-Humans, pubmed-meshheading:9458733-Lymphokines, pubmed-meshheading:9458733-Microcirculation, pubmed-meshheading:9458733-Models, Cardiovascular, pubmed-meshheading:9458733-Nitric Oxide, pubmed-meshheading:9458733-Nitric Oxide Synthase, pubmed-meshheading:9458733-Oligonucleotides, Antisense, pubmed-meshheading:9458733-Rats, pubmed-meshheading:9458733-Renal Artery, pubmed-meshheading:9458733-Umbilical Veins, pubmed-meshheading:9458733-Vascular Endothelial Growth Factor A, pubmed-meshheading:9458733-Vascular Endothelial Growth Factors, pubmed-meshheading:9458733-Wound Healing
pubmed:year
1998
pubmed:articleTitle
Podokinesis in endothelial cell migration: role of nitric oxide.
pubmed:affiliation
Department of Medicine, State University of New York, Stony Brook 11794-8152, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't