Linked Life Data

11423573

Source:http://linkedlifedata.com/resource/pubmed/id/11423573

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2001-6-25
pubmed:abstractText
Impaired angiogenesis and decreased vascular endothelial growth factor (VEGF) expression were recently documented in the remnant kidney (RK) model of progressive renal failure. VEGF (50 microg/kg, twice daily) was administered to RK rats between weeks 4 and 8 after surgery, and rats were euthanized at week 8 for histologic study. During the administration of VEGF (n = 7) or vehicle (n = 6), systemic BP was comparable in the two groups. VEGF treatment resulted in improved renal function and lower mortality rates, compared with the vehicle-treated group. Renal histologic analyses confirmed a 3.5-fold increase in glomerular endothelial cell proliferation (0.14 +/- 0.03 versus 0.04 +/- 0.02 proliferating endothelial cells/glomerulus, VEGF versus vehicle, P < 0.05), a twofold increase in peritubular capillary endothelial cell proliferation (1.60 +/- 0.30 versus 0.78 +/- 0.17 cells/mm(2), VEGF versus vehicle, P < 0.01), a threefold decrease in peritubular capillary rarefaction (P < 0.01), and a twofold increase in endothelial nitrix oxide synthase expression (P < 0.05) in the VEGF-treated group; an eightfold increase in urinary nitrate/nitrite levels (P < 0.05) was also noted. Although the difference in glomerulosclerosis scores did not reach statistical significance (0.67 +/- 0.42 versus 1.22 +/- 0.63, VEGF versus vehicle; range, 0 to 4; P = NS), VEGF-treated rats exhibited less interstitial collagen type III deposition (9.32 +/- 3.26 versus 17.45 +/- 7.50%, VEGF versus vehicle, P < 0.01) and reduced tubular epithelial cell injury, as manifested by osteopontin expression (5.57 +/- 1.60 versus 9.58 +/- 3.45%, VEGF versus vehicle, P < 0.01). In conclusion, VEGF treatment reduces fibrosis and stabilizes renal function in the RK model. The use of angiogenic factors may represent a new approach to the treatment of kidney disease.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1046-6673
pubmed:author
pubmed:issnType
Print
pubmed:volume
12
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1448-57
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:11423573-Animals, pubmed-meshheading:11423573-Blood Pressure, pubmed-meshheading:11423573-Capillaries, pubmed-meshheading:11423573-Endothelial Growth Factors, pubmed-meshheading:11423573-Fibrosis, pubmed-meshheading:11423573-Glomerulosclerosis, Focal Segmental, pubmed-meshheading:11423573-Kidney, pubmed-meshheading:11423573-Kidney Diseases, pubmed-meshheading:11423573-Kidney Glomerulus, pubmed-meshheading:11423573-Kidney Tubules, pubmed-meshheading:11423573-Lymphokines, pubmed-meshheading:11423573-Macrophages, pubmed-meshheading:11423573-Male, pubmed-meshheading:11423573-Neovascularization, Physiologic, pubmed-meshheading:11423573-Nephrectomy, pubmed-meshheading:11423573-Nitric Oxide Synthase, pubmed-meshheading:11423573-Nitrites, pubmed-meshheading:11423573-Rats, pubmed-meshheading:11423573-Rats, Sprague-Dawley, pubmed-meshheading:11423573-Renal Circulation, pubmed-meshheading:11423573-Time Factors, pubmed-meshheading:11423573-Vascular Endothelial Growth Factor A, pubmed-meshheading:11423573-Vascular Endothelial Growth Factors
pubmed:year
2001
pubmed:articleTitle
Impaired angiogenesis in the remnant kidney model: II. Vascular endothelial growth factor administration reduces renal fibrosis and stabilizes renal function.
pubmed:affiliation
Division of Nephrology, University of Washington, Seattle, WA, USA. dkang@bcm.tmc.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't