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Title: Reciprocal interactions between endothelial cells and macrophages in angiogenic vascular niches

Abstract

The ability of macrophages to promote vascular growth has been associated with the secretion and local delivery of classic proangiogenic factors (e.g., VEGF-A and proteases). More recently, a series of studies have also revealed that physical contact of macrophages with growing blood vessels coordinates vascular fusion of emerging sprouts. Interestingly, the interactions between macrophages and vascular endothelial cells (ECs) appear to be bidirectional, such that activated ECs also support the expansion and differentiation of proangiogenic macrophages from myeloid progenitors. Here, we discuss recent findings suggesting that dynamic angiogenic vascular niches might also exist in vivo, e.g. in tumors, where sprouting blood vessels and immature myeloid cells like monocytes engage in heterotypic interactions that are required for angiogenesis. Finally, we provide an account of emerging mechanisms of cell-to-cell communication that rely on secreted microvesicles, such as exosomes, which can offer a vehicle for the rapid exchange of molecules and genetic information between macrophages and ECs engaged in angiogenesis. -- Highlights: • Macrophages promote angiogenesis by secreting proangiogenic factors. • Macrophages modulate angiogenesis via cell-to-cell contacts with endothelial cells. • Endothelial cells promote the differentiation of proangiogenic macrophages. • Macrophages and endothelial cells may cooperate to form angiogenic vascular niches.

Authors:
;  [1];  [1];  [2];  [1]
  1. The Swiss Institute for Experimental Cancer Research (ISREC), School of Life Sciences, Swiss Federal Institute of Technology Lausanne (EPFL), 1015 Lausanne (Switzerland)
  2. (United States)
Publication Date:
OSTI Identifier:
22267814
Resource Type:
Journal Article
Resource Relation:
Journal Name: Experimental Cell Research; Journal Volume: 319; Journal Issue: 11; Other Information: Copyright (c) 2013 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA)
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; ANGIOGENESIS; BLOOD VESSELS; FIBROBLASTS; GROWTH FACTORS; MACROPHAGES; MONOCYTES

Citation Formats

Baer, Caroline, Squadrito, Mario Leonardo, Iruela-Arispe, M. Luisa, E-mail: arispe@mcdb.ucla.edu, Department of Molecular, Cell and Developmental Biology and Molecular Biology Institute, University of California, Los Angeles 90095, CA, and De Palma, Michele, E-mail: michele.depalma@epfl.ch. Reciprocal interactions between endothelial cells and macrophages in angiogenic vascular niches. United States: N. p., 2013. Web. doi:10.1016/J.YEXCR.2013.03.026.
Baer, Caroline, Squadrito, Mario Leonardo, Iruela-Arispe, M. Luisa, E-mail: arispe@mcdb.ucla.edu, Department of Molecular, Cell and Developmental Biology and Molecular Biology Institute, University of California, Los Angeles 90095, CA, & De Palma, Michele, E-mail: michele.depalma@epfl.ch. Reciprocal interactions between endothelial cells and macrophages in angiogenic vascular niches. United States. doi:10.1016/J.YEXCR.2013.03.026.
Baer, Caroline, Squadrito, Mario Leonardo, Iruela-Arispe, M. Luisa, E-mail: arispe@mcdb.ucla.edu, Department of Molecular, Cell and Developmental Biology and Molecular Biology Institute, University of California, Los Angeles 90095, CA, and De Palma, Michele, E-mail: michele.depalma@epfl.ch. Mon . "Reciprocal interactions between endothelial cells and macrophages in angiogenic vascular niches". United States. doi:10.1016/J.YEXCR.2013.03.026.
@article{osti_22267814,
title = {Reciprocal interactions between endothelial cells and macrophages in angiogenic vascular niches},
author = {Baer, Caroline and Squadrito, Mario Leonardo and Iruela-Arispe, M. Luisa, E-mail: arispe@mcdb.ucla.edu and Department of Molecular, Cell and Developmental Biology and Molecular Biology Institute, University of California, Los Angeles 90095, CA and De Palma, Michele, E-mail: michele.depalma@epfl.ch},
abstractNote = {The ability of macrophages to promote vascular growth has been associated with the secretion and local delivery of classic proangiogenic factors (e.g., VEGF-A and proteases). More recently, a series of studies have also revealed that physical contact of macrophages with growing blood vessels coordinates vascular fusion of emerging sprouts. Interestingly, the interactions between macrophages and vascular endothelial cells (ECs) appear to be bidirectional, such that activated ECs also support the expansion and differentiation of proangiogenic macrophages from myeloid progenitors. Here, we discuss recent findings suggesting that dynamic angiogenic vascular niches might also exist in vivo, e.g. in tumors, where sprouting blood vessels and immature myeloid cells like monocytes engage in heterotypic interactions that are required for angiogenesis. Finally, we provide an account of emerging mechanisms of cell-to-cell communication that rely on secreted microvesicles, such as exosomes, which can offer a vehicle for the rapid exchange of molecules and genetic information between macrophages and ECs engaged in angiogenesis. -- Highlights: • Macrophages promote angiogenesis by secreting proangiogenic factors. • Macrophages modulate angiogenesis via cell-to-cell contacts with endothelial cells. • Endothelial cells promote the differentiation of proangiogenic macrophages. • Macrophages and endothelial cells may cooperate to form angiogenic vascular niches.},
doi = {10.1016/J.YEXCR.2013.03.026},
journal = {Experimental Cell Research},
number = 11,
volume = 319,
place = {United States},
year = {Mon Jul 01 00:00:00 EDT 2013},
month = {Mon Jul 01 00:00:00 EDT 2013}
}
  • Highlights: •Angiogenic activities were reduced in iPSECs from MMD patients. •Many mitosis-regulated genes were downregulated in iPSECs from MMD patients. •RNF213 R4810K downregulated Securin and inhibited angiogenic activity. •Securin suppression by siRNA reduced angiogenic activities of iPSECs and HUVECs. -- Abstract: Moyamoya disease (MMD) is a cerebrovascular disease characterized by occlusive lesions in the circle of Willis. The RNF213 R4810K polymorphism increases susceptibility to MMD. Induced pluripotent stem cells (iPSCs) were established from unaffected fibroblast donors with wild-type RNF213 alleles, and from carriers/patients with one or two RNF213 R4810K alleles. Angiogenic activities of iPSC-derived vascular endothelial cells (iPSECs) from patientsmore » and carriers were lower (49.0 ± 19.4%) than from wild-type subjects (p < 0.01). Gene expression profiles in iPSECs showed that Securin was down-regulated (p < 0.01) in carriers and patients. Overexpression of RNF213 R4810K downregulated Securin, inhibited angiogenic activity (36.0 ± 16.9%) and proliferation of humanumbilical vein endothelial cells (HUVECs) while overexpression of RNF213 wild type did not. Securin expression was downregulated using RNA interference techniques, which reduced the level of tube formation in iPSECs and HUVECs without inhibition of proliferation. RNF213 R4810K reduced angiogenic activities of iPSECs from patients with MMD, suggesting that it is a promising in vitro model for MMD.« less
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