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Endothelial cell FGF signaling is required for injury response but not for vascular homeostasis
Journal article   Open access

Endothelial cell FGF signaling is required for injury response but not for vascular homeostasis

Sunday S Oladipupo, Craig Smith, Andrea Santeford, Changwon Park, Abdoulaye Sene, Luke A Wiley, Patrick Osei-Owusu, Joann Hsu, Nicole Zapata, Fang Liu, …
Proceedings of the National Academy of Sciences - PNAS, v 111(37), pp 13379-13384
16 Sep 2014
PMID: 25139991
url
https://doi.org/10.1073/pnas.1324235111View
Published, Version of Record (VoR)Maybe Open Access (Publisher Bronze) Open

Abstract

Animals Animals, Newborn Blood Vessels - pathology Capillary Permeability Endothelial Cells - metabolism Enzyme Activation Eye - pathology Fibroblast Growth Factors - metabolism Hematopoiesis Homeostasis Hypoxia - metabolism Hypoxia - pathology Integrases - metabolism Mice Neovascularization, Pathologic - metabolism Neovascularization, Pathologic - pathology Neovascularization, Physiologic Receptors, Fibroblast Growth Factor - metabolism Signal Transduction Stress, Physiological Vascular Endothelial Growth Factor Receptor-2 - metabolism Wound Healing
Endothelial cells (ECs) express fibroblast growth factor receptors (FGFRs) and are exquisitely sensitive to FGF signals. However, whether the EC or another vascular cell type requires FGF signaling during development, homeostasis, and response to injury is not known. Here, we show that Flk1-Cre or Tie2-Cre mediated deletion of FGFR1 and FGFR2 (Fgfr1/2(Flk1-Cre) or Fgfr1/2(Tie2-Cre) mice), which results in deletion in endothelial and hematopoietic cells, is compatible with normal embryonic development. As adults, Fgfr1/2(Flk1-Cre) mice maintain normal blood pressure and vascular reactivity and integrity under homeostatic conditions. However, neovascularization after skin or eye injury was significantly impaired in both Fgfr1/2(Flk1-Cre) and Fgfr1/2(Tie2-Cre) mice, independent of either hematopoietic cell loss of FGFR1/2 or vascular endothelial growth factor receptor 2 (Vegfr2) haploinsufficiency. Also, impaired neovascularization was associated with delayed cutaneous wound healing. These findings reveal a key requirement for cell-autonomous EC FGFR signaling in injury-induced angiogenesis, but not for vascular homeostasis, identifying the EC FGFR signaling pathway as a target for diseases associated with aberrant vascular proliferation, such as age-related macular degeneration, and for modulating wound healing without the potential toxicity associated with direct manipulation of systemic FGF or VEGF activity.

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Cell Biology
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