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In the MSU-induced GA mouse model, complement C5a was secreted as a primary chemotactic signal for neutrophils (77), which could then bind to the G protein-coupled receptors to generate calcium ion flux (79), thereby mediating vesicle fusion with the cell membrane and promoting the secretion of exosomes coated with LTB4 (80)

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These layers progressively became more damaged toward the end of the 2 and 4 weeks (Figure 6, Figure 7)