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CCR2 recruits an inflammatory macrophage subpopulation critical for angiogenesis in tissue repair

Sebastian Willenborg, Tina Lucas, Geert van Loo UGent, Johanna A Knipper, Thomas Krieg, Ingo Haase, Bent Brachvogel, Matthias Hammerschmidt, Andras Nagy and Napoleone Ferrara, et al. (2012) BLOOD. 120(3). p.613-625
abstract
Monocytes/macrophages are critical in orchestrating the tissue-repair response. However, the mechanisms that govern macrophage regenerative activities during the sequential phases of repair are largely unknown. In the present study, we examined the dynamics and functions of diverse monocyte/macrophage phenotypes during the sequential stages of skin repair. By combining the analysis of a new CCR2-eGFP reporter mouse model with conditional mouse mutants defective in myeloid cell-restricted CCR2 signaling or VEGF-A synthesis, we show herein that among the large number of inflammatory CCR2(+)Ly6C(+) macrophages that dominate the early stage of repair, only a small fraction strongly expresses VEGF-A that has nonredundant functions for the induction of vascular sprouts. The switch of macrophage-derived VEGF-A during the early stage of tissue growth toward epidermal-derived VEGF-A during the late stage of tissue maturation was critical to achieving physiologic tissue vascularization and healing progression. The results of the present study provide new mechanistic insights into CCR2-mediated recruitment of blood monocyte subsets into damaged tissue, the dynamics and functional consequences of macrophage plasticity during the sequential repair phases, and the complementary role of macrophage-derived VEGF-A in coordinating effective tissue growth and vascularization in the context of tissue-resident wound cells. Our findings may be relevant for novel monocyte-based therapies to promote tissue vascularization.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
VEGF, BONE-MARROW, MONOCYTES, WOUND REPAIR, MYELOID CELLS, PROMOTER ACTIVITY, ENDOTHELIAL-GROWTH-FACTOR, MICE, REGENERATION, METASTASIS
journal title
BLOOD
Blood
volume
120
issue
3
pages
613 - 625
Web of Science type
Article
Web of Science id
000307440100018
JCR category
HEMATOLOGY
JCR impact factor
9.06 (2012)
JCR rank
3/66 (2012)
JCR quartile
1 (2012)
ISSN
0006-4971
DOI
10.1182/blood-2012-01-403386
project
Ghent researchers on unfolded proteins in inflammatory disease (GROUP-ID)
project
Ghent researchers on unfolded proteins in inflammatory disease (GROUP-ID)
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
3053583
handle
http://hdl.handle.net/1854/LU-3053583
date created
2012-11-15 12:18:30
date last changed
2014-05-12 11:02:03
@article{3053583,
  abstract     = {Monocytes/macrophages are critical in orchestrating the tissue-repair response. However, the mechanisms that govern macrophage regenerative activities during the sequential phases of repair are largely unknown. In the present study, we examined the dynamics and functions of diverse monocyte/macrophage phenotypes during the sequential stages of skin repair. By combining the analysis of a new CCR2-eGFP reporter mouse model with conditional mouse mutants defective in myeloid cell-restricted CCR2 signaling or VEGF-A synthesis, we show herein that among the large number of inflammatory CCR2(+)Ly6C(+) macrophages that dominate the early stage of repair, only a small fraction strongly expresses VEGF-A that has nonredundant functions for the induction of vascular sprouts. The switch of macrophage-derived VEGF-A during the early stage of tissue growth toward epidermal-derived VEGF-A during the late stage of tissue maturation was critical to achieving physiologic tissue vascularization and healing progression. The results of the present study provide new mechanistic insights into CCR2-mediated recruitment of blood monocyte subsets into damaged tissue, the dynamics and functional consequences of macrophage plasticity during the sequential repair phases, and the complementary role of macrophage-derived VEGF-A in coordinating effective tissue growth and vascularization in the context of tissue-resident wound cells. Our findings may be relevant for novel monocyte-based therapies to promote tissue vascularization.},
  author       = {Willenborg, Sebastian and Lucas, Tina and van Loo, Geert and Knipper, Johanna A and Krieg, Thomas and Haase, Ingo and Brachvogel, Bent and Hammerschmidt, Matthias and Nagy, Andras and Ferrara, Napoleone and Pasparakis, Manolis and Eming, Sabine A},
  issn         = {0006-4971},
  journal      = {BLOOD},
  keyword      = {VEGF,BONE-MARROW,MONOCYTES,WOUND REPAIR,MYELOID CELLS,PROMOTER ACTIVITY,ENDOTHELIAL-GROWTH-FACTOR,MICE,REGENERATION,METASTASIS},
  language     = {eng},
  number       = {3},
  pages        = {613--625},
  title        = {CCR2 recruits an inflammatory macrophage subpopulation critical for angiogenesis in tissue repair},
  url          = {http://dx.doi.org/10.1182/blood-2012-01-403386},
  volume       = {120},
  year         = {2012},
}

Chicago
Willenborg, Sebastian, Tina Lucas, Geert van Loo, Johanna A Knipper, Thomas Krieg, Ingo Haase, Bent Brachvogel, et al. 2012. “CCR2 Recruits an Inflammatory Macrophage Subpopulation Critical for Angiogenesis in Tissue Repair.” Blood 120 (3): 613–625.
APA
Willenborg, S., Lucas, T., van Loo, G., Knipper, J. A., Krieg, T., Haase, I., Brachvogel, B., et al. (2012). CCR2 recruits an inflammatory macrophage subpopulation critical for angiogenesis in tissue repair. BLOOD, 120(3), 613–625.
Vancouver
1.
Willenborg S, Lucas T, van Loo G, Knipper JA, Krieg T, Haase I, et al. CCR2 recruits an inflammatory macrophage subpopulation critical for angiogenesis in tissue repair. BLOOD. 2012;120(3):613–25.
MLA
Willenborg, Sebastian, Tina Lucas, Geert van Loo, et al. “CCR2 Recruits an Inflammatory Macrophage Subpopulation Critical for Angiogenesis in Tissue Repair.” BLOOD 120.3 (2012): 613–625. Print.