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Osteoblasts Regulate Angiogenesis in Response to Mechanical Unloading.

Vimal Veeriah1, Riccardo Paone1, Suvro Chatterjee2,3

  • 1Department of Biotechnological and Applied Clinical Sciences, University of L'Aquila, via Vetoio - Coppito 2, 67100, L'aquila, Italy.

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Summary
This summary is machine-generated.

Mechanical unloading of bone affects endothelial cells. Unloaded osteoblasts release vascular endothelial growth factor (VEGF), promoting angiogenesis, which is crucial in disuse osteoporosis.

Keywords:
AngiogenesisEndothelial cellsMechanical unloadingOsteoblastVEGF

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Area of Science:

  • Bone biology
  • Endothelial cell biology
  • Angiogenesis

Background:

  • Mechanical unloading of bone leads to reduced osteogenesis and increased resorption.
  • Endothelial cells play a role in bone remodeling.
  • The response of endothelial cells to unloaded osteoblasts is not fully understood.

Purpose of the Study:

  • To investigate the feedback response of endothelial cells to unloaded osteoblasts.
  • To determine the role of vascular endothelial growth factor (VEGF) in this process.
  • To elucidate the contribution of osteoblast-endothelial cell crosstalk to disuse osteoporosis.

Main Methods:

  • Primary endothelial cells, mouse aortic rings, and chicken egg yolk membranes were incubated with conditioned medium from unloaded osteoblasts.
  • In vivo disuse osteoporosis was induced in mice using botulinum toxin A (Botox).
  • The effect of VEGF inhibition using avastin was assessed.

Main Results:

  • Unloaded osteoblasts upregulated VEGF production.
  • Osteoblast-conditioned medium enhanced endothelial cell viability, proliferation, migration, and tube formation in vitro.
  • Conditioned medium promoted ex vivo endothelial cell sprouting and in ovo angiogenesis.
  • VEGF inhibition blocked the pro-angiogenic effects of unloaded osteoblast-conditioned medium.
  • Botox-induced bone unloading led to VEGF overexpression in osteoblasts.

Conclusions:

  • Osteoblasts under mechanical unloading upregulate VEGF, stimulating angiogenesis.
  • This osteoblast-endothelial cell crosstalk is a key factor in the endothelial response during disuse osteoporosis.
  • VEGF is a significant mediator of angiogenesis in the context of disuse osteoporosis.