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CYR61/CCN1 Regulates Sclerostin Levels and Bone Maintenance.

Gexin Zhao1, Bau-Lin Huang2, Diana Rigueur1

  • 1Department of Orthopaedic Surgery, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA.

Journal of Bone and Mineral Research : the Official Journal of the American Society for Bone and Mineral Research
|January 20, 2018
PubMed
Summary

CYR61/CCN1 protein is crucial for maintaining bone mass by regulating osteoblast and osteocyte function. Its absence leads to decreased bone density, altered vasculature, and disrupted Wnt signaling, impacting bone health.

Keywords:
ANIMAL MODELSBONE MODELING AND REMODELINGCELL/TISSUE SIGNALINGCELLS OF BONEGENETIC ANIMAL MODELSMOLECULAR PATHWAYSOSTEOCYTESPARACRINE PATHWAYSREMODELINGWNT/BETA-CATENIN/LRPS

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Area of Science:

  • Biochemistry
  • Bone Biology
  • Extracellular Matrix Biology

Background:

  • CYR61/CCN1 is a matricellular protein involved in regulating bone healing and osteogenic differentiation.
  • Its precise role in bone development and maintenance in vivo remains to be fully elucidated.

Purpose of the Study:

  • To investigate the physiological role of CYR61/CCN1 in bone development and maintenance using a bone-specific knockout mouse model.
  • To elucidate the mechanisms by which CYR61/CCN1 influences bone mass, including its effects on osteoblast/osteocyte function and associated signaling pathways.

Main Methods:

  • Generation of Cyr61 bone-specific conditional knockout mice.
  • Extensive analysis of trabecular and cortical bone mass, bone vasculature, and osteoclast number in knockout and wild-type littermates.
  • In vitro assays using UMR-106 osteosarcoma cells to assess the role of CYR61/CCN1 in Sost expression and Wnt signaling.

Main Results:

  • Cyr61 conditional knockout mice exhibited significantly reduced trabecular and cortical bone mass compared to wild-type controls.
  • Key changes observed include increased RankL expression (leading to more osteoclasts), decreased VegfA expression (reducing bone vasculature), and increased Sost expression (inhibiting Wnt signaling).
  • In vitro studies demonstrated that CYR61/CCN1 suppresses Sost expression, and blocking Sost can restore Wnt responsiveness in knockout cells.

Conclusions:

  • CYR61/CCN1 plays a critical role in regulating mature osteoblast and osteocyte function to maintain bone mass.
  • It exerts its effects through both angiogenic mechanisms (via VegfA) and modulation of Wnt signaling, partly through the regulation of the Wnt antagonist Sost.
  • These findings highlight CYR61/CCN1 as a potential therapeutic target for bone diseases characterized by low bone mass.