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Endothelium-specific ablation of PDGFB leads to pericyte loss and glomerular, cardiac and placental abnormalities

Journal article
Authors Mattias Bjarnegård
Maria Enge
Jenny Norlin
Sigrun Gustafsdottir
Simon Fredriksson
Alexandra Abramsson
Minoru Takemoto
Erika Gustafsson
Reinhard Fassler
Christer Betsholtz
Published in DEVELOPMENT
Volume 131
Issue 8
Pages 1847-1857
ISSN 0950-1991
Publication year 2004
Published at Institute of Medical Biochemistry
Pages 1847-1857
Language en
Links dx.doi.org/10.1242/dev.01080
Keywords smooth-muscle-cells, retinal vascular patterns, protease-activated ligand, central-nervous-system, growth-factor, diabetic-retinopathy, beta-receptor, in-vivo, b-chain, kidney glomeruli
Subject categories Developmental Biology

Abstract

Platelet-derived growth factor-B (PDGFB) is necessary for normal cardiovascular development, but the relative importance of different cellular sources of PDGFB has not been established. Using Cre-lox techniques, we show here that genetic ablation of Pdgfb in endothelial cells leads to impaired recruitment of pericytes to blood vessels. The endothelium-restricted Pdgfb knockout mutants also developed organ defects including cardiac, placental and renal abnormalities. These defects were similar to those observed in Pdgfb null mice. However, in marked contrast to the embryonic lethality of Pdgfb null mutants, the endothelium-specific mutants survived into adulthood with persistent pathological changes, including brain microhemorrhages, focal astrogliosis, and kidney glomerulus abnormalities. This spectrum of pathological changes is reminiscent of diabetic microangiopathy, suggesting that the endothelium-restricted Pdgfb knockouts may serve as models for some of the pathogenic events of vascular complications to diabetes. Key words: PDGFB, Endothelium, Cre, loxP, Pericytes, Microaneurysm

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