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Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl...
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The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
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STING inhibition accelerates the bone healing process while enhancing type H vessel formation.

Xiaojun Chen1, Wenxin He2, Mengzhe Sun1

  • 1Department of Plastic and Reconstructive Surgery, Shanghai Ninth People's Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, China.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|October 25, 2021
PubMed
Summary

Stimulator of interferon genes (STING) activation hinders bone healing and blood vessel formation. Inhibiting STING accelerates bone repair and promotes type H vessel development, crucial for osteogenesis.

Keywords:
angiogenesisbone healingstimulator of interferon genestype H vessels

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Area of Science:

  • Immunology
  • Vascular Biology
  • Bone Biology

Background:

  • The stimulator of interferon genes (STING) is a key innate immunity factor linked to angiogenesis.
  • Type H vessels are a specific subtype of bone vasculature critical for bone healing.

Purpose of the Study:

  • To investigate the role of STING in angiogenesis and type H vessel formation during bone healing.
  • To evaluate the therapeutic potential of modulating STING activity for bone repair.

Main Methods:

  • In vitro assays using human umbilical vein endothelial cells to assess STING's effect on angiogenesis.
  • Ex vivo metatarsal experiments and in vivo mouse models of bone fracture/defect.
  • Radiography, micro-CT, and histological analyses (cryosection, paraffin section) to evaluate bone healing, type H vessel formation, and osteogenesis.

Main Results:

  • STING activation inhibited angiogenesis in vitro and ex vivo, and slowed bone healing in vivo, characterized by increased callus, reduced type H vessels, and impaired mineralization.
  • STING inhibition using H-151 (human) or C-176 (mouse) promoted angiogenesis and enhanced type H vessel formation.
  • Inhibition of STING led to improved bone healing metrics, including higher bone volume density and increased osteocalcin (OCN)-positive cells.

Conclusions:

  • STING plays a dual role in bone healing, with activation impeding the process.
  • Inhibiting STING accelerates bone healing by promoting angiogenesis and type H vessel formation.
  • Targeting STING represents a promising therapeutic strategy for enhancing bone repair.