Research articles
ScienceAsia 48 (2022):ID 697-704 |doi:
10.2306/scienceasia1513-1874.2022.098
Lipopolysaccharide promotes the osteoclastogenesis through
the autophagic degradationof TNF receptor-associated factor 3
Jing Hua, Xianyou Zenga, Chengcheng Songb,*, Lei Zhangb,*
ABSTRACT: Lipopolysaccharide (LPS) is a pro-osteoclastogenic factor and autophagic activator. TNF receptorassociated factor (TRAF) 3, an anti-osteoclastogenic factor, can be degraded by autophagic activation. The effect of
LPS on the level of TRAF3 during the osteoclastogenesis keeps vague. In this study, we investigated the roles of LPS in
the expression patterns of TRAF3 in vivo and in vitro. Combined with the application of autophagic pharmacological
inhibitors, we observed the significance of LPS-regulated autophagy in TRAF3 protein level. Moreover, we explored
the effects of TRAF3 on LPS-induced osteoclastogenesis using gain-of-function and loss-of-function assays in vitro.
Our study showed that LPS could reduce the protein level of TRAF3 in osteoclast precursors (OCPs) in vitro and in
vivo, while no affecting the mRNA expression of TRAF3. In addition, TRAF3 overexpression reversed LPS-induced
osteoclastogenesis. Importantly, LPS-inhibited TRAF3 protein level was recovered by autophagic inhibition with
chloroquine or bafilomycin. Furthermore, LPS-induced osteoclastogenesis was suppressed by chloroquine, which was
reversed by TRAF3 silencing. In conclusion, LPS can promote the autophagic degradation of TRAF3, which serves as
an indispensable underlying mechanism in LPS-induced osteoclastogenesis
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Department of Stomatology, The Affiliated Hospital of Jinggangshan University, Ji?an, Jiangxi 343000 China
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Department of Stomatology, Dujiangyan people?s Hospital, Chengdu, Sichuang 611800 China |
* Corresponding author, E-mail: SCCDJY@yeah.net, 282772709@qq.com
Received 23 Oct 2021, Accepted 27 Feb 2022
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