Linked Life Data

9836521

Source:http://linkedlifedata.com/resource/pubmed/id/9836521

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
1998-12-21
pubmed:abstractText
The formation of new microvasculature by capillary sprouting at the site of islet transplantation is crucial for the long-term survival and function of the graft. Vascular endothelial growth factor (VEGF), an endothelial cell-specific mitogen with potent angiogenic and vascular permeability-inducing properties, may be a key factor in modulating the revascularization of islets after transplantation. In this study, we examined the gene expression of VEGF mRNA in three tumor cell lines and in isolated whole and dispersed rat islets in vitro by Northern blot hybridization in normoxic (5% CO2, 95% humidified air) and hypoxic (1% O2, 5% CO2, 94% N2) culture conditions. Increased expression of VEGF mRNA was observed in beta-TC3, RAW 264.7, and IC-21 tumor cell lines when subjected to hypoxia. With isolated whole islets in normoxic culture, a threefold increase in VEGF mRNA (P < 0.001) was seen at 48 h as compared with freshly isolated islets. This response was similar to the 3.8-fold increase observed with islets subjected to hypoxia. Dispersed rat islet cell clusters cultured on Matrigel for 24 h under hypoxic conditions showed a 3.4-fold increase (P < 0.01) in VEGF mRNA compared with those cultured in normoxia. This correlated with increased VEGF secretion as determined by enzyme-linked immunosorbent assay. Immunohistochemical studies revealed the presence of increased expression of VEGF protein near the center of islets after 24 h of normoxic culture. Islet cell clusters on Matrigel showed intense cellular localization of VEGF in both beta-cells and non-beta-cells. These findings suggest that rat islet cells, when subjected to hypoxia during the first few days after transplantation, may act as a major source of VEGF, thereby initiating revascularization and maintaining the vascular permeability of the grafted islets.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0012-1797
pubmed:author
pubmed:issnType
Print
pubmed:volume
47
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1894-903
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:9836521-Animals, pubmed-meshheading:9836521-Anoxia, pubmed-meshheading:9836521-Biocompatible Materials, pubmed-meshheading:9836521-Cell Line, Transformed, pubmed-meshheading:9836521-Collagen, pubmed-meshheading:9836521-Drug Combinations, pubmed-meshheading:9836521-Endothelial Growth Factors, pubmed-meshheading:9836521-Fluorescent Antibody Technique, pubmed-meshheading:9836521-Gene Expression Regulation, pubmed-meshheading:9836521-Islets of Langerhans, pubmed-meshheading:9836521-Laminin, pubmed-meshheading:9836521-Lymphokines, pubmed-meshheading:9836521-Mice, pubmed-meshheading:9836521-Proteoglycans, pubmed-meshheading:9836521-RNA, Messenger, pubmed-meshheading:9836521-Rats, pubmed-meshheading:9836521-Rats, Sprague-Dawley, pubmed-meshheading:9836521-Tumor Cells, Cultured, pubmed-meshheading:9836521-Vascular Endothelial Growth Factor A, pubmed-meshheading:9836521-Vascular Endothelial Growth Factors
pubmed:year
1998
pubmed:articleTitle
Hypoxia induces vascular endothelial growth factor gene and protein expression in cultured rat islet cells.
pubmed:affiliation
Joslin Diabetes Center, Department of Medicine, Harvard Medical School, Boston, Massachusetts 02215, USA.
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't