J Bone Metab.  2021 Aug;28(3):223-230. 10.11005/jbm.2021.28.3.223.

Anti-Müllerian Hormone Negatively Regulates Osteoclast Differentiation by Suppressing the Receptor Activator of Nuclear Factor-κB Ligand Pathway

Affiliations
  • 1Department of Pharmacology, Chonnam National University Medical School, Gwangju, Korea
  • 2Hard-Tissue Biointerface Research Center, School of Dentistry, Chonnam National University, Gwangju, Korea
  • 3Aging Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, Korea
  • 4Department of Functional Genomics, KRIBB School of Bioscience, Korea University of Science and Technology, Daejeon, Korea

Abstract

Background
Multiple members of the transforming growth factor-β (TGF-β) superfamily have well-established roles in bone homeostasis. Anti-Müllerian hormone (AMH) is a member of TGF-β superfamily of glycoproteins that is responsible for the regression of fetal Müllerian ducts and the transcription inhibition of gonadal steroidogenic enzymes. However, the involvement of AMH in bone remodeling is unknown. Therefore, we investigated whether AMH has an effect on bone cells as other TGF-β superfamily members do.
Methods
To identify the roles of AMH in bone cells, we administered AMH during osteoblast and osteoclast differentiation, cultured the cells, and then stained the cultured cells with Alizarin red and tartrate-resistant acid phosphatase, respectively. We analyzed the expression of osteoblast- or osteoclast-related genes using real-time polymerase chain reaction and western blot.
Results
AMH does not affect bone morphogenetic protein 2-mediated osteoblast differentiation but inhibits receptor activator of nuclear factor-κB (NF-κB) ligand-induced osteoclast differentiation. The inhibitory effect of AMH on osteoclast differentiation is mediated by IκB-NF-κB signaling.
Conclusions
AMH negatively regulates osteoclast differentiation without affecting osteoblast differentiation.

Keyword

Anti-müllerian hormone; Osteoblasts; Osteoclasts; TGF-beta superfamily proteins
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