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Background <p> Heterotopic ossification (HO) is an abnormal tissue repair program that occurs after musculoskeletal injury and involves the formation of ectopic bone within soft tissues, and the cellular and molecular mechanisms underlying its development are currently unclear.</p> Methods <p> We investigated the relationship between local inflammatory microenvironment and osteogenic differentiation of mesenchymal progenitor cells (MPC) in trauma-induced HO mice by single-cell transcriptomics.</p> Results <p>We revealed diverse phenotypes of MPCs and macrophages in HO, and showed that macrophage-derived <i>Osm</i> was associated with aberrant chondrogenic progenitor cell differentiation. Furthermore, <i>Spi1</i>, as a novel regulator of early macrophage activation and regulation of <i>Osm</i> expression in HO, which activates M1 macrophages after initial injury thereby contributing to HO formation.</p> Conclusions <p>Our findings provide novel insights into understanding the functional impact of macrophages on MPC fate, and we also believe that this may offer new therapeutic opportunities to reduce HO risk by targeting macrophage-driven aberrant progenitor cell differentiation.</p>

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Single cell RNA-seq analysis associates Osm signaling in macrophages with osteogenic differentiation during heterotopic ossification

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月28日

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  • Jian Wang,
  • Jiangwei Fan,
  • Xiaohui Yang

摘要

Background

Heterotopic ossification (HO) is an abnormal tissue repair program that occurs after musculoskeletal injury and involves the formation of ectopic bone within soft tissues, and the cellular and molecular mechanisms underlying its development are currently unclear.

Methods

We investigated the relationship between local inflammatory microenvironment and osteogenic differentiation of mesenchymal progenitor cells (MPC) in trauma-induced HO mice by single-cell transcriptomics.

Results

We revealed diverse phenotypes of MPCs and macrophages in HO, and showed that macrophage-derived Osm was associated with aberrant chondrogenic progenitor cell differentiation. Furthermore, Spi1, as a novel regulator of early macrophage activation and regulation of Osm expression in HO, which activates M1 macrophages after initial injury thereby contributing to HO formation.

Conclusions

Our findings provide novel insights into understanding the functional impact of macrophages on MPC fate, and we also believe that this may offer new therapeutic opportunities to reduce HO risk by targeting macrophage-driven aberrant progenitor cell differentiation.