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The atherogenic Scarb1 null mouse model shows a high bone mass phenotype.

Corine Martineau1, Louise Martin-Falstrault, Louise Brissette

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Summary

Scavenger receptor class B, type I (SR-BI) deficiency in mice increases bone mass by enhancing bone formation. These mice, contrary to expectations, are not prone to osteoporosis despite altered cholesterol metabolism.

Keywords:
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Area of Science:

  • Biochemistry
  • Bone Biology
  • Metabolic Disease

Background:

  • Scavenger receptor class B, type I (SR-BI) facilitates cholesteryl ester uptake from high-density lipoproteins (HDL), crucial for cholesterol transport and excretion.
  • SR-BI deficiency is linked to atherosclerosis, and a connection between atherosclerosis and osteoporosis exists.
  • The role of SR-BI in bone metabolism remains largely uncharacterized.

Purpose of the Study:

  • To investigate the impact of SR-BI deficiency on bone metabolism and bone mass.
  • To characterize bone morphometry and cellular functions of marrow stromal cells (MSCs) in SR-BI null mice.

Main Methods:

  • Utilized microcomputed tomography and histology for bone morphometry assessment.
  • Isolated and cultured marrow stromal cells (MSCs) from wild-type and Scarb1 null mice for in vitro functional assays.
  • Analyzed cholesterol levels, proliferation rates, alkaline phosphatase activity, mineralization potential, and gene expression (Osterix/Sp7, Caveolin-1/Cav1).

Main Results:

  • SR-BI null mice exhibited increased total and HDL-associated cholesterol.
  • Significant increases in bone volume fraction and trabecular number were observed in null mice.
  • Enhanced osteoblast surface, mineralizing surface, and bone formation rate were evident in null mice.
  • In vitro, MSCs from null mice showed increased proliferation, alkaline phosphatase activity, and mineralization potential, with altered Sp7 and Cav1 expression.
  • Scarb1 knockout impaired HDL-dependent regulation of Cav1 gene expression.

Conclusions:

  • SR-BI null mice do not develop osteoporosis; instead, they display higher bone mass.
  • Enhanced bone formation, driven by increased osteoblast activity and MSC function, contributes to the higher bone mass.
  • SR-BI plays a role in regulating bone cell function and potentially bone mass, independent of its direct role in HDL cholesterol uptake by MSCs.