Local H2 release remodels senescence microenvironment for improved repair of injured bone
Shengqiang Chen,
Yuanman Yu,
Songqing Xie,
Danna Liang,
Wei Shi,
Sizhen Chen,
Guanglin Li,
Wei Tang (),
Changsheng Liu () and
Qianjun He ()
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Shengqiang Chen: Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences
Yuanman Yu: East China University of Science and Technology
Songqing Xie: Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences
Danna Liang: Shenzhen University
Wei Shi: Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences
Sizhen Chen: Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences
Guanglin Li: Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences
Wei Tang: Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences
Changsheng Liu: East China University of Science and Technology
Qianjun He: Shanghai Jiao Tong University
Nature Communications, 2023, vol. 14, issue 1, 1-16
Abstract:
Abstract The senescence microenvironment, which causes persistent inflammation and loss of intrinsic regenerative abilities, is a main obstacle to effective tissue repair in elderly individuals. In this work, we find that local H2 supply can remodel the senescence microenvironment by anti-inflammation and anti-senescence effects in various senescent cells from skeletally mature bone. We construct a H2-releasing scaffold which can release high-dosage H2 (911 mL/g, up to 1 week) by electrospraying polyhydroxyalkanoate-encapsulated CaSi2 nanoparticles onto mesoporous bioactive glass. We demonstrate efficient remodeling of the microenvironment and enhanced repair of critical-size bone defects in an aged mouse model. Mechanistically, we reveal that local H2 release alters the microenvironment from pro-inflammation to anti-inflammation by senescent macrophages repolarization and secretome change. We also show that H2 alleviates the progression of aging/injury-superposed senescence, facilitates the recruitment of endogenous cells and the preservation of their regeneration capability, thereby creating a pro-regenerative microenvironment able to support bone defect regeneration.
Date: 2023
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:14:y:2023:i:1:d:10.1038_s41467-023-43618-z
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DOI: 10.1038/s41467-023-43618-z
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