Lipopolysaccharide inhibits osteoblast formation and receptor activator of nuclear factor-κB ligand degradation via autophagy inhibition.

IF 1.3 4区 医学 Q4 ENDOCRINOLOGY & METABOLISM Endocrine journal Pub Date : 2024-04-30 Epub Date: 2024-03-14 DOI:10.1507/endocrj.EJ23-0484
Huaizhi Zhang, Jianhua Lin, Xu Chen, Jianhui Dai, Haibin Lin
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Abstract

Lipopolysaccharide (LPS) and Receptor Activator of Nuclear Factor-κB Ligand (RANKL) are the two important factors causing bone loss, which is an important pathogenesis for osteoporosis. However, the relationship between LPS and RANKL is not yet clear. LPS can be involved in the weakened osteoblast formation as an autophagy regulator, and osteoblasts and their precursors are the source cells for RANKL production. Our study aimed to explore the relationship between autophagy changes and RANKL production during LPS-regulated osteoblasts. Our results showed that LPS inhibited autophagy (LC3 conversion and autophagosome formation) and enhanced the protein and mRNA expression of RANKL in MC3T3-E1 osteoblast precursor line. Autophagy upregulation with Rapamycin over BECN1 overexpression rescued LPS-inhibited osteoblast formation and -promoted RANKL protein production in MC3T3-E1 cells. In vivo experiments supported that damaged bone mass, bone microstructure, osteoblastic activity (ALP and P1NP production by ELISA assays) and enhanced RANKL production by LPS administration were partially rescued by Rapamycin application. In conclusion, LPS can inhibit autophagy in osteoblast precursors, thereby inhibiting osteoblast formation and RANKL autophagic degradation.

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脂多糖通过抑制自噬作用抑制成骨细胞的形成和核因子κB受体激活剂配体的降解。
脂多糖(LPS)和核因子κB受体活化配体(RANKL)是导致骨质流失的两个重要因素,也是骨质疏松症的一个重要发病机制。然而,LPS 和 RANKL 之间的关系尚不明确。LPS 可作为自噬调节因子参与成骨细胞的形成,而成骨细胞及其前体是 RANKL 生成的来源细胞。我们的研究旨在探讨 LPS 调节成骨细胞过程中自噬变化与 RANKL 生成之间的关系。结果显示,LPS抑制了MC3T3-E1成骨细胞前体系的自噬(LC3转化和自噬体形成),并增强了RANKL的蛋白和mRNA表达。用雷帕霉素上调自噬,再加上 BECN1 的过表达,可挽救 LPS 抑制的成骨细胞形成,并促进 MC3T3-E1 细胞中 RANKL 蛋白的产生。体内实验证明,应用雷帕霉素可部分缓解 LPS 对骨质量、骨微观结构、成骨细胞活性(通过 ELISA 方法检测 ALP 和 P1NP 的产生)的破坏,并促进 RANKL 的产生。总之,LPS 可抑制成骨细胞前体的自噬,从而抑制成骨细胞的形成和 RANKL 的自噬降解。
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来源期刊
Endocrine journal
Endocrine journal 医学-内分泌学与代谢
CiteScore
4.30
自引率
5.00%
发文量
224
审稿时长
1.5 months
期刊介绍: Endocrine Journal is an open access, peer-reviewed online journal with a long history. This journal publishes peer-reviewed research articles in multifaceted fields of basic, translational and clinical endocrinology. Endocrine Journal provides a chance to exchange your ideas, concepts and scientific observations in any area of recent endocrinology. Manuscripts may be submitted as Original Articles, Notes, Rapid Communications or Review Articles. We have a rapid reviewing and editorial decision system and pay a special attention to our quick, truly scientific and frequently-citable publication. Please go through the link for author guideline.
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