Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
14
pubmed:dateCreated
2005-12-1
pubmed:abstractText
Pericyte loss and capillary regression are characteristic for incipient diabetic retinopathy. Pericyte recruitment is involved in vessel maturation, and ligand-receptor systems contributing to pericyte recruitment are survival factors for endothelial cells in pericyte-free in vitro systems. We studied pericyte recruitment in relation to the susceptibility toward hyperoxia-induced vascular remodeling using the pericyte reporter X-LacZ mouse and the mouse model of retinopathy of prematurity (ROP). Pericytes were found in close proximity to vessels, both during formation of the superficial and the deep capillary layers. When exposure of mice to the ROP was delayed by 24 h, i.e., after the deep retinal layer had formed [at postnatal (p) day 8], preretinal neovascularizations were substantially diminished at p18. Mice with a delayed ROP exposure had 50% reduced avascular zones. Formation of the deep capillary layers at p8 was associated with a combined up-regulation of angiopoietin-1 and PDGF-B, while VEGF was almost unchanged during the transition from a susceptible to a resistant capillary network. Inhibition of Tie-2 function either by soluble Tie-2 or by a sulindac analog, an inhibitor of Tie-2 phosphorylation, resensitized retinal vessels to neovascularizations due to a reduction of the deep capillary network. Inhibition of Tie-2 function had no effect on pericyte recruitment. Our data indicate that the final maturation of the retinal vasculature and its resistance to regressive signals such as hyperoxia depend on the completion of the multilayer structure, in particular the deep capillary layers, and are independent of the coverage by pericytes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1530-6860
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
19
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2035-6
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:16215210-Angiopoietin-1, pubmed-meshheading:16215210-Animals, pubmed-meshheading:16215210-Anoxia, pubmed-meshheading:16215210-Capillaries, pubmed-meshheading:16215210-Cell Survival, pubmed-meshheading:16215210-Densitometry, pubmed-meshheading:16215210-Diabetic Retinopathy, pubmed-meshheading:16215210-Endothelium, Vascular, pubmed-meshheading:16215210-Genes, Reporter, pubmed-meshheading:16215210-Immunoblotting, pubmed-meshheading:16215210-Lac Operon, pubmed-meshheading:16215210-Ligands, pubmed-meshheading:16215210-Mice, pubmed-meshheading:16215210-Neovascularization, Pathologic, pubmed-meshheading:16215210-Pericytes, pubmed-meshheading:16215210-Phosphorylation, pubmed-meshheading:16215210-Platelet-Derived Growth Factor, pubmed-meshheading:16215210-Receptor, TIE-2, pubmed-meshheading:16215210-Retina, pubmed-meshheading:16215210-Retinal Vessels, pubmed-meshheading:16215210-Time Factors, pubmed-meshheading:16215210-Up-Regulation
pubmed:year
2005
pubmed:articleTitle
Endothelial survival factors and spatial completion, but not pericyte coverage of retinal capillaries determine vessel plasticity.
pubmed:affiliation
Medical Clinic and Policlinic 3, Justus-Liebig University Giessen, Giessen, Germany. hans-peter.hammes@med5.ma.uni-heidelberg.de
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't