ROS Activated NETosis of Bone Marrow CD55
Abstract
Neutrophil NETosis is markedly dysregulated in the aging body. Bone marrow serves as the powerhouse of neutrophil differentiation, while the state of neutrophil NETosis therein and its relationship with bone aging remains largely elusive. Moreover, it remains unclear how neutrophil heterogeneity and pro-inflammatory cues within bone marrow synergistically regulate neutrophil NETosis. Here, we find neutrophil NETosis is highly activated in the bone marrow of 3-mon male senescence-accelerated mouse prone 6 (SAMP6), and the released NETs induce BMSCs senescence and impairs their osteogenesis. Further, we verify in vivo NETs-clearance significantly ameliorates bone aging of 3-mon male SAMP6 mice. Next, through scRNA-seq we find a CD55
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Research summary
Neutrophil NETosis in the bone marrow contributes to senescence of bone marrow stem cells and impairs osteogenesis in aging mice. This study addresses mechanisms of aging by exploring how neutrophil activity affects bone health, which is a critical aspect of longevity research.
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