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Tanguay, Adam P.; Menon, Nikhil G.; Boudreau, Margaret H.; Jastrzebski, Sandra; Woods, Paige S.; Doyle, Erica A.; Edwards, W. Brent; Jay, Gregory D.; Deymier, Alix C.; Lorenzo, Joseph; Lee, Sun‐Kyeong; Schmidt, Tannin A.

PRG4 deficiency in mice alters skeletal structure, mechanics, and calvarial osteoclastogenesis, and rhPRG4 inhibits in vitro osteoclastogenesis

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  • Medientyp: E-Artikel
  • Titel: PRG4 deficiency in mice alters skeletal structure, mechanics, and calvarial osteoclastogenesis, and rhPRG4 inhibits in vitro osteoclastogenesis
  • Beteiligte: Tanguay, Adam P.; Menon, Nikhil G.; Boudreau, Margaret H.; Jastrzebski, Sandra; Woods, Paige S.; Doyle, Erica A.; Edwards, W. Brent; Jay, Gregory D.; Deymier, Alix C.; Lorenzo, Joseph; Lee, Sun‐Kyeong; Schmidt, Tannin A.
  • Erschienen: Wiley, 2024
  • Erschienen in: Journal of Orthopaedic Research, 42 (2024) 6, Seite 1231-1243
  • Sprache: Englisch
  • DOI: 10.1002/jor.25772
  • ISSN: 0736-0266; 1554-527X
  • Entstehung:
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  • Beschreibung: <jats:title>Abstract</jats:title><jats:p>Osteoporosis is a chronic disease characterized by reduced bone mass and increased fracture risk, estimated to affect over 10 million people in the United States alone. Drugs used to treat bone loss often come with significant limitations and/or long‐term safety concerns. Proteoglycan‐4 (PRG4, also known as lubricin) is a mucin‐like glycoprotein best known for its boundary lubricating function of articular cartilage. In more recent years, it has been shown that PRG4 has anti‐inflammatory properties, contributes to the maintenance of subchondral bone integrity, and patients with <jats:italic>PRG4</jats:italic> mutations are osteopenic. However, it remains unknown how PRG4 impacts mechanical and material properties of bone. Therefore, our objective was to perform a phenotyping study of bone in a <jats:italic>Prg4</jats:italic> gene trap (GT) mouse (PRG4 deficient). We found that femurs of <jats:italic>Prg4</jats:italic> GT mice have altered mechanical, structural, and material properties relative to wildtype littermates. Additionally, <jats:italic>Prg4</jats:italic> GT mice have a greater number of calvarial osteoclasts than wildtype mice, but do not have a notable inflammatory serum profile. Finally, <jats:italic>Prg4</jats:italic> GT mice do not have an altered rate of bone formation, and exogenous recombinant human PRG4 (rhPRG4) administration inhibited osteoclastogenesis in vitro, suggesting that the skeletal phenotype may be due to changes in bone resorption. Overall, this work demonstrates that PRG4 deficiency affects several integral properties of bone structure, mechanics, and skeletal cell activity, and provides the foundation and insight toward future work evaluating PRG4 as a potential therapeutic target in treating bone loss.</jats:p>