What question did this study set out to answer?

The study aims to explore how lincRNA-EPS influences osteoclastogenesis and bone resorption in the context of inflammation.

April 4, 2026Cell Death and Disease0 citationsOpen Access

LincRNA-EPS alleviates osteoclastogenesis under inflammatory microenvironment through preventing excessive iron metabolism

JWJin WangTongji University YWYabing WangTongji University ZZZhanwei ZhangTongji University

Key Points

The study aims to explore how lincRNA-EPS influences osteoclastogenesis and bone resorption in the context of inflammation.
Utilized lincRNA-EPS knockout mice to assess bone resorption under inflammatory conditions.
Conducted transcriptomics and protein sequencing to analyze osteoclastogenesis and iron homeostasis.
Implemented knockdown of lcn2 in osteoclast precursors to evaluate effects on iron metabolism and osteoclast differentiation.
LincRNA-EPS knockout worsened LPS-induced alveolar bone resorption and osteoclast differentiation.
Dysregulation of osteoclastogenesis and iron metabolism was observed without lincRNA-EPS, indicated by increased lcn2 expression.
Reducing lcn2 levels in wildtype mice alleviated bone loss due to periodontitis, but had no effect in KO mice.

Abstract

Abstract The precise regulation of bone homeostasis and the balance between bone resorption and formation in periodontitis remain unclear. This study explores the role of long intergenic noncoding RNA-erythroid prosurvival (lincRNA-EPS) in inflammatory osteoclastogenesis and bone resorption. LincRNA-EPS knockout (KO) worsened LPS-induced alveolar bone resorption in vivo and osteoclast differentiation in vitro. Transcriptomics and protein sequencing showed dysregulated osteoclastogenesis and iron homeostasis without lincRNA-EPS, marked by increased expression of Lcn2 . Knockdown of Lcn2 in osteoclast precursors (OCPs) resulted in a reduction in the level of iron metabolism and osteoclastogenesis; however, the regulatory response was delayed in KO cells. Correspondingly, overexpression of lincRNA-EPS accelerated the regulation of iron metabolism. Further, reducing Lcn2 levels in wildtype mice alleviated periodontitis-related bone loss, but not in KO mice. Taken together, we identified the critical role of lincRNA-EPS in regulating osteoclastogenesis under inflammatory environment, by preventing excessive iron metabolism caused by Lcn2.

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