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VEGF coordinates interaction of pericytes and endothelial cells during vasculogenesis and experimental angiogenesis
Author(s) -
Hagedorn Martin,
Balke Maurice,
Schmidt Annette,
Bloch Wilhelm,
Kurz Haymo,
Javerzat Sophie,
Rousseau Benoît,
Wilting Joerg,
Bikfalvi Andreas
Publication year - 2004
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.20020
Subject(s) - biology , vasculogenesis , desmin , angiogenesis , microbiology and biotechnology , vascular endothelial growth factor , pericyte , embryoid body , chorioallantoic membrane , arteriogenesis , vascular endothelial growth factor a , endothelial stem cell , progenitor cell , immunology , in vitro , stem cell , cancer research , vimentin , vegf receptors , immunohistochemistry , biochemistry , adult stem cell
Biological activities of vascular endothelial growth factor (VEGF) have been studied extensively in endothelial cells (ECs), but few data are available regarding its effects on pericytes. In murine embryoid body cultures, VEGF‐induced expression of desmin and α‐smooth muscle actin (α‐SMA) in CD‐31 + cells. The number of CD‐31 + /desmin + vascular chords increased with VEGF treatment time and peaked during a differentiation window between 6 and 9 days after plating. In vivo, VEGF‐induced elongation and migration of desmin‐positive pericytes and coverage of angiogenic capillaries, as revealed by analysis of Sambucus nigra lectin‐stained vascular beds of the chick chorioallantoic membrane. VEGF also caused significant decrease of intercapillary spaces, an indicator for intussusceptive vascular growth. These VEGF‐mediated effects point at a more intricate interaction between ECs and pericytes cells than previously demonstrated and suggest that pericytes may be derived from EC progenitors in vitro and not only stabilize capillaries but also participate in vascular remodeling in vivo. Developmental Dynamics 230:23–33, 2004. © 2004 Wiley‐Liss, Inc.