Osteoblast expression of vascular endothelial growth factor is modulated by the extracellular microenvironment.

@article{Spector2001OsteoblastEO,
  title={Osteoblast expression of vascular endothelial growth factor is modulated by the extracellular microenvironment.},
  author={Jason A. Spector and Babak J. Mehrara and Joshua A. Greenwald and Pierre B. Saadeh and Douglas S. Steinbrech and Pierre J. Bouletreau and L P Smith and Michael T. Longaker},
  journal={American journal of physiology. Cell physiology},
  year={2001},
  volume={280 1},
  pages={
          C72-80
        }
}
Angiogenesis, the formation of new blood vessels, is crucial to the process of fracture healing. Vascular disruption after osseous injury results in an acidic, hypoxic wound environment. We have previously shown that osteoblasts can produce vascular endothelial growth factor (VEGF) in response to a variety of stimuli. In this study we examined pH and lactate concentration, two components of the putative fracture extracellular microenvironment, and determined their relative contribution to… 

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  • 2017
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In this review, the properties of VEGF and its receptors that are relevant to bone formation and repair are summarized; the roles of V EGF during development of endochondral and membranous bones; and the contributions of VegF to bone healing during different phases of bone repair are discussed.
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Mesenchymal stem cell proliferation and mineralization but not osteogenic differentiation are strongly affected by extracellular pH.
VEGF and bone cell signalling: an essential vessel for communication?
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A means of understanding the directionality of VEGF signalling in adult bone would allow us to most effectively target angiogenic pathways in diseases characterized by changes in bone remodelling rates and enhance bone repair when compromised.
Constitutive and inducible expression and regulation of vascular endothelial growth factor.
Acidic pH stimulates the production of the angiogenic CXC chemokine, CXCL8 (interleukin‐8), in human adult mesenchymal stem cells via the extracellular signal‐regulated kinase, p38 mitogen‐activated protein kinase, and NF‐κB pathways
TLDR
The use of specific mitogen‐activated protein kinase (MAPK) signal transduction inhibitors indicated that the pH‐dependent increase in CXCL8 mRNA is due to activation of ERK and p38 pathways, and the JNK pathway was not involved.
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