Linked Life Data

16389944

Source:http://linkedlifedata.com/resource/pubmed/id/16389944

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2006-1-4
pubmed:abstractText
Angiogenesis is a promising target for the development of effective strategies for the treatment of malignant brain tumors in that it has the potential to starve large tumors and prevent the regrowth of residual margins. Two critical steps in angiogenesis, the proliferation of activated endothelial cells and their migration into the perivascular space (sprouting), require adherence of the endothelial cells to the extracellular matrix (ECM). Thus, the availability of the appropriate ligands within the ECM contributes to the regulation of angiogenesis. In addition, several components of the ECM can act through other mechanisms to further promote angiogenesis or inhibit it. Current evidence suggests that the regulation of angiogenesis is a dynamic process in which the endothelial cells can promote angiogenesis by secreting proteases that remodel the ECM, tumor cells can further promote angiogenesis by secreting ECM components and actively remodeling their environment, and stromal cells may respond to angiogenesis associated with tumors and inflammatory reactions by secreting inhibitory molecules. Here, we provide a critical review of the protein and proteoglycan components of the ECM that have been implicated in angiogenesis with an emphasis on their role in promoting or inhibiting angiogenesis in brain tumors.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1015-6305
pubmed:author
pubmed:issnType
Print
pubmed:volume
15
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
318-26
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
The role of the extracellular matrix in angiogenesis in malignant glioma tumors.
pubmed:affiliation
Department of Pathology, Division of Neuropathology, University of Alabama at Birmingham, Birmingham, AL 35294-0007, USA.
pubmed:publicationType
Journal Article, Review, Research Support, N.I.H., Extramural