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Glechoma hederacea Suppresses RANKL-mediated Osteoclastogenesis

Authors
 J.K. Hwang  ;  M. Erkhembaatar  ;  D.R. Gu  ;  S.H. Lee  ;  C.H. Lee  ;  D.M. Shin  ;  Y.R. Lee  ;  M.S. Kim 
Citation
 JOURNAL OF DENTAL RESEARCH, Vol.93(7) : 685-690, 2014 
Journal Title
 JOURNAL OF DENTAL RESEARCH 
ISSN
 0022-0345 
Issue Date
2014
MeSH
Acid Phosphatase/drug effects ; Animals ; Bone Marrow Cells/drug effects ; Calcium Channel Blockers/pharmacology ; Calcium Channels/drug effects ; Calcium Signaling/drug effects ; Cell Differentiation/drug effects ; Cells, Cultured ; Cytosol/drug effects ; Dihydropyridines/pharmacology ; Dose-Response Relationship, Drug ; Giant Cells/drug effects ; Isoenzymes/drug effects ; Lamiaceae* ; Macrophages/drug effects ; Mice ; Mice, Inbred C57BL ; NFATC Transcription Factors/drug effects ; Osteoclasts/drug effects* ; Plant Extracts/pharmacology* ; RANK Ligand/drug effects* ; Tartrate-Resistant Acid Phosphatase
Keywords
NFATc1 ; [Ca2+]i oscillation ; bone remodeling ; natural product ; osteoclast ; periodontitis
Abstract
Glechoma hederacea (GH), commonly known as ground-ivy or gill-over-the-ground, has been extensively used in folk remedies for relieving symptoms of inflammatory disorders. However, the molecular mechanisms underlying the therapeutic action of GH are poorly understood. Here, we demonstrate that GH constituents inhibit osteoclastogenesis by abrogating receptor activator of nuclear κ-B ligand (RANKL)-induced free cytosolic Ca2+ ([Ca2+]i) oscillations. To evaluate the effect of GH on osteoclastogenesis, we assessed the formation of multi-nucleated cells (MNCs), enzymatic activity of tartrate-resistant acidic phosphatase (TRAP), expression of nuclear factor of activated T-cells cytoplasmic 1 (NFATc1), and [Ca2+]i alterations in response to treatment with GH ethanol extract (GHE) in primarily cultured bone marrow-derived macrophages (BMMs). Treatment of RANKL-stimulated or non-stimulated BMMs with GHE markedly suppressed MNC formation, TRAP activity, and NFATc1 expression in a dose-dependent manner. Additionally, GHE treatment induced a large transient elevation in [Ca2+]i while suppressing RANKL-induced [Ca2+]i oscillations, which are essential for NFATc1 activation. GHE-evoked increase in [Ca2+]i was dependent on extracellular Ca2+ and was inhibited by 1,4-dihydropyridine (DHP), inhibitor of voltage-gated Ca2+ channels (VGCCs), but was independent of store-operated Ca2+ channels. Notably, after transient [Ca2+] elevation, treatment with GHE desensitized the VGCCs, resulting in an abrogation of RANKL-induced [Ca2+]i oscillations and MNC formation. These findings demonstrate that treatment of BMMs with GHE suppresses RANKL-mediated osteoclastogenesis by activating and then desensitizing DHP-sensitive VGCCs, suggesting potential applications of GH in the treatment of bone disorders, such as periodontitis, osteoporosis, and rheumatoid arthritis.
Full Text
http://jdr.sagepub.com/content/93/7/685.long
DOI
10.1177/0022034514536579
Appears in Collections:
2. College of Dentistry (치과대학) > Dept. of Oral Biology (구강생물학교실) > 1. Journal Papers
Yonsei Authors
Shin, Dong Min(신동민) ORCID logo https://orcid.org/0000-0001-6042-0435
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/99103
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