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N16 suppresses RANKL-mediated osteoclatogenesis by down-regulating RANK expression.

Authors
  • Lin, Jia-Bi1
  • Wu, Hao1
  • Liu, Yu-Ling1
  • Shaw, Pang-Chui2
  • Li, Pei-Bo3
  • 1 Guangdong Engineering and Technology Research Center for Quality and Efficacy Re-evaluation of Post-marketed TCM, Guangdong Key Laboratory of Plant Resources, School of Life Sciences, Sun Yat-sen University, Guangzhou, People's Republic of China. , (China)
  • 2 State Key Laboratory of Research on Bioactivities and Clinical Applications of Medicinal Plants (CUHK), LDS YYC R & D Centre for Chinese Medicine and School of Life Sciences, The Chinese University of Hong Kong, Hong Kong, China. , (China)
  • 3 Guangdong Engineering and Technology Research Center for Quality and Efficacy Re-evaluation of Post-marketed TCM, Guangdong Key Laboratory of Plant Resources, School of Life Sciences, Sun Yat-sen University, Guangzhou, People's Republic of China. Electronic address: [email protected] , (China)
Type
Published Article
Journal
International journal of biological macromolecules
Publication Date
Nov 18, 2019
Identifiers
DOI: 10.1016/j.ijbiomac.2019.10.159
PMID: 31751723
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

N16 is an active protein existing in Pinctada martensi. Our previous studies have demonstrated that N16 inhibited osteoclast differentiation in vitro. To better understand how N16 regulates osteoclast differentiation, RAW264.7 cells, a murine monocytic cell line and murine bone marrow-derived macrophages (BMMs) were adopted. Treatment of RAW264.7 cells with RANKL activated osteoclastogenesis and N16 inhibited the formation of multinucleated osteoclasts and TRAP activity. The suppression occurred at the early stage of osteoclastogenesis. Moreover, we found that N16 inhibited PU.1 and MITF expressions, mirroring the inhibition of RANK expressions, indicating that N16 inhibited RANK expression by down-regulating the expressions of MITF and PU.1, thus preventing osteoclastogenesis. Copyright © 2019 Elsevier B.V. All rights reserved.

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