Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2002-2-8
pubmed:abstractText
Interactions among growth factors, cells, and extracellular matrix regulate proliferation during normal development and in pathologies such as atherosclerosis. SPARC (secreted protein, acidic, and rich in cysteine) is a matrix-associated glycoprotein that modulates the adhesion and proliferation of vascular cells. In this study, we demonstrate that SPARC inhibits human arterial smooth muscle cell proliferation stimulated by platelet-derived growth factor or by adhesion to monomeric type I collagen. Binding studies with SPARC and SPARC peptides indicate specific and saturable interaction with smooth muscle cells that involves the C-terminal Ca2+-binding region of the protein. We also report that SPARC arrests monomeric collagen-supported smooth muscle cell proliferation in the late G1-phase of the cell cycle in the absence of an effect on cell shape or on levels of cyclin-dependent kinase inhibitors. Cyclin-dependent kinase-2 activity, p107 and cyclin A levels, and retinoblastoma protein phosphorylation are markedly reduced in response to the addition of exogenous SPARC and/or peptides derived from specific domains of SPARC. Thus, SPARC, previously characterized as an inhibitor of platelet-derived growth factor binding to its receptor, also antagonizes smooth muscle cell proliferation mediated by monomeric collagen at the level of cyclin-dependent kinase-2 activity.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0730-2312
pubmed:author
pubmed:copyrightInfo
Copyright 2002 Wiley-Liss, Inc.
pubmed:issnType
Print
pubmed:volume
84
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
759-71
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:11835401-Amino Acid Sequence, pubmed-meshheading:11835401-Animals, pubmed-meshheading:11835401-Aorta, pubmed-meshheading:11835401-Cell Cycle, pubmed-meshheading:11835401-Cell Division, pubmed-meshheading:11835401-Cell Size, pubmed-meshheading:11835401-Collagen Type I, pubmed-meshheading:11835401-Cyclin-Dependent Kinases, pubmed-meshheading:11835401-Drug Interactions, pubmed-meshheading:11835401-Enzyme Inhibitors, pubmed-meshheading:11835401-Extracellular Matrix, pubmed-meshheading:11835401-G1 Phase, pubmed-meshheading:11835401-Humans, pubmed-meshheading:11835401-Mice, pubmed-meshheading:11835401-Molecular Sequence Data, pubmed-meshheading:11835401-Muscle, Smooth, Vascular, pubmed-meshheading:11835401-Osteonectin, pubmed-meshheading:11835401-Peptides, pubmed-meshheading:11835401-Phosphorylation, pubmed-meshheading:11835401-Platelet-Derived Growth Factor, pubmed-meshheading:11835401-Retinoblastoma Protein
pubmed:year
2002
pubmed:articleTitle
Inhibition of PDGF-stimulated and matrix-mediated proliferation of human vascular smooth muscle cells by SPARC is independent of changes in cell shape or cyclin-dependent kinase inhibitors.
pubmed:affiliation
Department of Vascular Biology, The Hope Heart Institute, Seattle, Washington 98104, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't