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Psychosine inhibits osteoclastogenesis and bone resorption via G protein-coupled receptor 65

S H Ahn1, S-Y Lee, J-E Baek

  • 1Division of Endocrinology and Metabolism, Asan Medical Center, University of Ulsan College of Medicine, 388-1 Poongnap-2Dong, Songpa-Gu, Seoul, 138-736, South Korea.

Journal of Endocrinological Investigation
|April 6, 2015
PubMed
Abstract

Insights

The lysosphingolipid psychosine inhibits bone loss by suppressing osteoclast formation and activity via G protein-coupled receptor 65 (GPR65). This mechanism involves increased intracellular cyclic adenosine monophosphate (cAMP) levels.

Area of Science:

  • Bone biology
  • Endocrinology
  • Pharmacology

Background:

  • G protein-coupled receptor 65 (GPR65) is implicated in suppressing ovariectomy-induced bone loss.
  • Lysosphingolipids are signaling molecules with diverse biological functions.

Purpose of the Study:

  • To investigate the effect of psychosine, a GPR65 ligand, on osteoclast differentiation and bone resorption.
  • To elucidate the molecular mechanism underlying psychosine's action on bone cells.

Main Methods:

  • Osteoclasts were differentiated from mouse bone marrow macrophages.
  • In vitro bone resorption was assessed using dentine discs.
  • Gene expression of osteoclast markers was analyzed by qRT-PCR.
  • GPR65 was knocked down using siRNA.
  • Intracellular cyclic adenosine monophosphate (cAMP) levels were measured.

Main Results:

  • Psychosine significantly inhibited osteoclastogenesis and in vitro bone resorption.
  • Psychosine decreased the expression of osteoclast differentiation markers.
  • Psychosine treatment led to increased intracellular cAMP levels.
  • GPR65 knockdown abrogated the effects of psychosine on osteoclastogenesis and cAMP levels.

Conclusions:

  • Psychosine inhibits osteoclastogenesis and bone resorption.
  • The inhibitory effect of psychosine is mediated through GPR65.
  • Increased intracellular cAMP levels are a key mechanism in psychosine's action.

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