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Biomed Rep. 2018 May;8(5):407-416. doi: 10.3892/br.2018.1075. Epub 2018 Mar 09.

Suppression of osteoclastogenesis via α2-adrenergic receptors.

Biomedical reports

Kosuke Hamajima, Kazunori Hamamura, Andy Chen, Hiroki Yokota, Hironori Mori, Shoyoku Yo, Hisataka Kondo, Kenjiro Tanaka, Kyoko Ishizuka, Daisuke Kodama, Takao Hirai, Ken Miyazawa, Shigemi Goto, Akifumi Togari

Affiliations

  1. Department of Pharmacology, School of Dentistry, Aichi-Gakuin University, Nagoya, Aichi 464-8650, Japan.
  2. Department of Orthodontics, School of Dentistry, Aichi-Gakuin University, Nagoya, Aichi 464-8650, Japan.
  3. Department of Biomedical Engineering, Indiana University - Purdue University Indianapolis, Indianapolis, IN 46202, USA.
  4. Laboratory of Neuropharmacology, School of Pharmacy, Aichi-Gakuin University, Nagoya, Aichi 464-8650, Japan.
  5. Laboratory of Medical Resources, School of Pharmacy, Aichi-Gakuin University, Nagoya, Aichi 464-8650, Japan.

PMID: 29725523 PMCID: PMC5920467 DOI: 10.3892/br.2018.1075

Abstract

The sympathetic nervous system is known to regulate osteoclast development. However, the involvement of α2-adrenergic receptors (α2-ARs) in osteoclastogenesis is not well understood. In the present study, their potential role in osteoclastogenesis was investigated. Guanabenz, clonidine and xylazine were used as agonists of α2-ARs, while yohimbine and idazoxan were employed as antagonists. Using RAW264.7 pre-osteoclast and primary bone marrow cells, the mRNA expression of the osteoclast-related genes nuclear factor of activated T-cells, cytoplasmic 1 (NFATc1), tartrate-resistant acid phosphatase (TRAP) and cathepsin K was evaluated following induction with receptor activator of nuclear factor κB ligand (RANKL). TRAP staining was also conducted to assess effects on osteoclastogenesis in mouse bone marrow cells

Keywords: agonist; antagonist; osteoclast; osteoclastogenesis; α2-adrenergic receptors

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