A plasticity window for blood vessel remodelling is defined by pericyte coverage of the preformed endothelial network and is regulated by PDGF-B and VEGF

Development. 1998 May;125(9):1591-8. doi: 10.1242/dev.125.9.1591.


Little is known about how the initial endothelial plexus is remodelled into a mature and functioning vascular network. Studying postnatal remodelling of the retina vasculature, we show that a critical step in vascular maturation, namely pericyte recruitment, proceeds by outmigration of cells positive for (alpha)-smooth muscle actin from arterioles and that coverage of primary and smaller branches lags many days behind formation of the endothelial plexus. The transient existence of a pericyte-free endothelial plexus coincides temporally and spatially with the process of hyperoxia-induced vascular pruning, which is a mechanism for fine tuning of vascular density according to available oxygen. Acquisition of a pericyte coating marks the end of this plasticity window. To substantiate that association with pericytes stabilizes the vasculature, endothelial-pericyte associations were disrupted by intraocular injection of PDGF-BB. Ectopic PDGF-BB caused the detachment of PDGF-beta receptor-positive pericytes from newly coated vessels, presumably through interference with endogenous cues, but had no effect on mature vessels. Disruption of endothelial-pericyte associations resulted in excessive regression of vascular loops and abnormal remodelling. Conversely, intraocular injection of VEGF accelerated pericyte coverage of the preformed endothelial plexus, thereby revealing a novel function of this pleiotropic angiogenic growth factor. These findings also provide a cellular basis for clinical observations that vascular regression in premature neonates subjected to oxygen therapy [i.e. in retinopathy of prematurity] drops precipitously upon maturation of retina vessels and a mechanistic explanation to our previous findings that VEGF can rescue immature vessels from hyperoxia-induced regression.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / analysis
  • Animals
  • Animals, Newborn
  • Arterioles / cytology
  • Becaplermin
  • Cell Movement
  • Endothelial Growth Factors / pharmacology*
  • Endothelium, Vascular / cytology
  • Endothelium, Vascular / growth & development*
  • Humans
  • Hyperoxia
  • Infant, Newborn
  • Lectins / analysis
  • Lymphokines / pharmacology*
  • Neovascularization, Physiologic / physiology*
  • Plant Lectins*
  • Platelet-Derived Growth Factor / pharmacology*
  • Proto-Oncogene Proteins c-sis
  • Rats
  • Receptors, Platelet-Derived Growth Factor / analysis
  • Retinal Vessels / growth & development*
  • Retinopathy of Prematurity / physiopathology
  • Vascular Endothelial Growth Factor A
  • Vascular Endothelial Growth Factors


  • Actins
  • Endothelial Growth Factors
  • Griffonia simplicifolia lectins
  • Lectins
  • Lymphokines
  • Plant Lectins
  • Platelet-Derived Growth Factor
  • Proto-Oncogene Proteins c-sis
  • Vascular Endothelial Growth Factor A
  • Vascular Endothelial Growth Factors
  • Becaplermin
  • Receptors, Platelet-Derived Growth Factor