Senescent-like macrophages mediate angiogenesis for endplate sclerosis via IL-10 secretion in male mice

Yonggang Fan, Weixin Zhang, Xiusheng Huang, Mingzhe Fan, Chenhao Shi, Lantian Zhao, Guofu Pi, Huafeng Zhang and Shuangfei Ni ()
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Yonggang Fan: 1st Affiliated Hospital of Zhengzhou University
Weixin Zhang: Zhejiang Chinese Medicine University
Xiusheng Huang: 1st Affiliated Hospital of Zhengzhou University
Mingzhe Fan: 1st Affiliated Hospital of Zhengzhou University
Chenhao Shi: 1st Affiliated Hospital of Zhengzhou University
Lantian Zhao: 1st Affiliated Hospital of Zhengzhou University
Guofu Pi: 1st Affiliated Hospital of Zhengzhou University
Huafeng Zhang: 1st Affiliated Hospital of Zhengzhou University
Shuangfei Ni: 1st Affiliated Hospital of Zhengzhou University

Nature Communications, 2024, vol. 15, issue 1, 1-21

Abstract: Abstract Endplate sclerosis is a notable aspect of spine degeneration or aging, but the mechanisms remain unclear. Here, we report that senescent macrophages accumulate in the sclerotic endplates of lumbar spine instability (LSI) or aging male mouse model. Specifically, knockout of cdkn2a (p16) in macrophages abrogates LSI or aging-induced angiogenesis and sclerosis in the endplates. Furthermore, both in vivo and in vitro studies indicate that IL-10 is the primary elevated cytokine of senescence-related secretory phenotype (SASP). Mechanistically, IL-10 increases pSTAT3 in endothelial cells, leading to pSTAT3 directly binding to the promoters of Vegfa, Mmp2, and Pdgfb to encourage their production, resulting in angiogenesis. This study provides information on understanding the link between immune senescence and endplate sclerosis, which might be useful for therapeutic approaches.

Date: 2024
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DOI: 10.1038/s41467-024-47317-1

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