Wnts heal by restraining angiogenesis.

Blood ·Vol. 121 ·No. 13 ·2013-03-28 ·Pages 2381-2

Kitajewski J

Abstract

暂无摘要

MeSH Terms

Animals Calcineurin/metabolism Macrophages/metabolism Neovascularization, Physiologic Vascular Endothelial Growth Factor Receptor-1/metabolism Wnt Signaling Pathway/physiology Wound Healing

Chemicals

Flt1 protein, mouse Vascular Endothelial Growth Factor Receptor-1 Calcineurin

Authors & Affiliations

1 authors, click to expand affiliations / ORCID

Kitajewski Jan

Columbia University Medical Center.

References (10)

10 references, click to expand

A transgenic mouse model of inducible macrophage depletion: effects of diphtheria toxin-driven lysozyme M-specific cell lineage ablation on wound inflammatory, angiogenic, and contractive processes.
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Regulation of angiogenesis by a non-canonical Wnt-Flt1 pathway in myeloid cells.
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Selective and specific macrophage ablation is detrimental to wound healing in mice.
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Macrophage Wnt-Calcineurin-Flt1 signaling regulates mouse wound angiogenesis and repair.
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Mice lacking Smad3 show accelerated wound healing and an impaired local inflammatory response.
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Notch1 deficiency results in decreased inflammation during wound healing and regulates vascular endothelial growth factor receptor-1 and inflammatory cytokine expression in macrophages.
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Tissue macrophages act as cellular chaperones for vascular anastomosis downstream of VEGF-mediated endothelial tip cell induction.
Blood. 2010 Aug 5;116(5):829-40 PMID: 20404134
Macrophages and angiogenesis: a role for Wnt signaling.
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Inflammatory cells during wound repair: the good, the bad and the ugly.
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Article Info

Journal

Blood

Abbr.

Blood

ISSN

1528-0020

DOI

10.1182/blood-2013-01-479063

Published

2013-03-28

Pages

2381-2

Language

English

Region

United States

NLM ID

7603509

PMCID

PMC3612850

Subset

Grants

NHLBI NIH HHS · R01 HL112626 · United States

Corrections

CommentOn

PMID: 23303818

External Links

PubMed source DOI: 10.1182/blood-2013-01-479063 PMC Full Text View journal details

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Wnts heal by restraining angiogenesis.

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