Linked Life Data

11297250

Source:http://linkedlifedata.com/resource/pubmed/id/11297250

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2001-4-11
pubmed:abstractText
Protease inhibitors regulate a variety of physiological and pathological processes including angiogenesis, embryo implantation, intravascular fibrinolysis, wound healing, and tumor invasion. Tissue factor pathway inhibitor (TFPI) 2 is a Mr 32,000 Kunitz-type serine protease inhibitor that inhibits plasmin, trypsin, chymotrypsin, cathepsin G, and plasma kallikrein but not urokinase-type plasminogen activator, tissue plasminogen activator, or thrombin. In this study, we determined the relative amounts of TFPI-2 in low-, intermediate-, and high-grade human glioma cell lines and tumor tissue samples. TFPI-2 protein and mRNA levels (measured by Western and Northern blotting) were highest in low-grade glioma cells (Hs683), lower in anaplastic astrocytoma cells (SW1088 and SW1783), and undetectable in high-grade glioma cells (SNB19). Analysis of TFPI-2 protein in human normal brain and in glioma tumor tissues for TFPI-2 revealed the highest levels in normal brain, lesser amounts in low-grade gliomas and anaplastic astrocytomas, and undetectable amounts in glioblastomas. In situ hybridization of TFPI-2 mRNA with normal brain tissues revealed the greatest positivity in neurons, with moderate positivity in both glial and endothelial cells and moderate, little, or no TFPI-2 mRNA in low-grade glioma, anaplastic astrocytoma, and glioblastoma tumor tissue samples, respectively. We also found that recombinant TFPI-2 inhibited the invasiveness of SNB19 glioblastoma cells in a Matrigel assay in a dose-dependent manner. Collectively, these results suggest that TFPI-2 has a regulatory role in the invasiveness of gliomas in vitro and in vivo.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1078-0432
pubmed:author
pubmed:issnType
Print
pubmed:volume
7
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
570-6
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:11297250-Astrocytoma, pubmed-meshheading:11297250-Blotting, Northern, pubmed-meshheading:11297250-Blotting, Western, pubmed-meshheading:11297250-Brain, pubmed-meshheading:11297250-Brain Neoplasms, pubmed-meshheading:11297250-Collagen, pubmed-meshheading:11297250-DNA, Complementary, pubmed-meshheading:11297250-Disease Progression, pubmed-meshheading:11297250-Dose-Response Relationship, Drug, pubmed-meshheading:11297250-Drug Combinations, pubmed-meshheading:11297250-Glioma, pubmed-meshheading:11297250-Glycoproteins, pubmed-meshheading:11297250-Humans, pubmed-meshheading:11297250-In Situ Hybridization, pubmed-meshheading:11297250-Laminin, pubmed-meshheading:11297250-Neurons, pubmed-meshheading:11297250-Proteoglycans, pubmed-meshheading:11297250-RNA, Messenger, pubmed-meshheading:11297250-Recombinant Proteins, pubmed-meshheading:11297250-Tumor Cells, Cultured
pubmed:year
2001
pubmed:articleTitle
Expression of tissue factor pathway inhibitor 2 inversely correlates during the progression of human gliomas.
pubmed:affiliation
Department of Neurosurgery, University of Texas M. D. Anderson Cancer Center, Houston 77030, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.