Tenascin-C promotes bone regeneration via inflammatory macrophages.

Qian Ren, Wenhui Xing, Bo Jiang, Heng Feng, Xuye Hu, Jinlong Suo, Lijun Wang, Weiguo Zou

State Key Laboratory of Cell Biology, Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.State Key Laboratory of Cell Biology, Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China. · pubmed

Paper

Abstract

During the early stage of tissue injury, macrophages play important roles in the activation of stem cells for further regeneration. However, the regulation of macrophages during bone regeneration remains unclear. Here, the extracellular matrix (ECM) tenascin-C (TNC) is found to express in the periosteum and recruit inflammatory macrophages. TNC-deficiency in the periosteum delays bone repair. Transplantation of macrophages derived from injured periosteum is able to rescue the decreased skeletal stem cells and impaired bone regeneration caused by TNC deficiency. The cell communication analysis identifies ITGA7 as a TNC receptor contributing to the recruitment of inflammatory macrophages. TNC expression declines in aged mice and the exogenous delivery of TNC significantly promotes bone regeneration after aging through the recruitment of macrophages. Taken together, this study reveals the regulation of macrophage recruitment and its function in the activation of skeletal stem cells after bone injury, providing a strategy to accelerate bone regeneration by TNC delivery.

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Research summary

The paper investigates the role of tenascin-C in bone regeneration and its interaction with inflammatory macrophages, particularly in the context of aging. By addressing the decline of TNC expression in aged mice and its implications for bone repair, the study touches on mechanisms that could be relevant to age-related decline in tissue regeneration. However, while it provides solid insights into the biology of bone healing, its impact on the broader field of longevity research is limited, as it primarily focuses on a specific aspect of tissue repair rather than a comprehensive approach to aging or lifespan extension.

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