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Osteoblasts secrete Cxcl9 to regulate angiogenesis in bone

Bin Huang1, Wenhao Wang1, Qingchu Li1

  • 1Academy of Orthopedics, Guangdong Province, Department of Orthopedics, The Third Affiliated Hospital, Southern Medical University, Guangzhou 510630, China.

Nature Communications
|December 15, 2016
PubMed

Insights

Osteoblasts secrete Cxcl9, an angiostatic factor that inhibits blood vessel formation and bone growth by blocking vascular endothelial growth factor. Targeting Cxcl9 may treat bone loss diseases.

Area of Science:

  • Bone biology
  • Angiogenesis
  • Cellular communication

Background:

  • Osteoblast-endothelial cell (EC) communication is crucial for bone remodeling.
  • Molecular mechanisms regulating this crosstalk are not fully understood.

Purpose of the Study:

  • To identify molecular factors involved in osteoblast-EC communication.
  • To elucidate the role of these factors in bone angiogenesis and osteogenesis.

Main Methods:

  • Identification of Cxcl9 as an osteoblast-secreted factor.
  • In vitro and in vivo experiments using mouse bone models.
  • Analysis of vascular endothelial growth factor (VEGF) interactions.
  • Investigation of mechanistic target of rapamycin complex 1 (mTORC1) signaling pathway.

Main Results:

  • Cxcl9, secreted by osteoblasts, acts as an angiostatic factor.
  • Cxcl9 inhibits angiogenesis and osteogenesis by interfering with VEGF binding to ECs and osteoblasts.
  • mTORC1 signaling upregulates Cxcl9 expression via STAT1, enhancing STAT1 binding to the Cxcl9 promoter.

Conclusions:

  • Osteoblast-derived Cxcl9 plays a critical role in regulating bone angiogenesis and osteogenesis.
  • Targeting Cxcl9 presents a potential therapeutic strategy to enhance bone angiogenesis and combat bone loss.

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