Kif15 regulates Coro1a+ cell migration and phagocytosis in zebrafish after spinal cord injury.

The role of immune cells is crucial in nerve regeneration following spinal cord injury. Kif15, a member of the kinesin family, has been shown to enhance macrophage phagocytosis. This study investigates the impact of Kif15 deficiency on immune cells in zebrafish with spinal cord injury. Using kif15 morphants in Tg(coro1a:EGFP) zebrafish, we observed increased recruitment of Coro1a+ cells to the injury site, followed by a rapid decline in kif15 morphants. Transcriptome analysis revealed that inflammatory and phagocytic signals were significantly enhanced at 1-hour post-injury (hpi), while MAPK pathways indicated growth at 24 hpi. Enhanced phagocytosis was confirmed using neutral red particles, and the Kif15 inhibitor GW406108X further supported increased migration and phagocytosis in macrophages. Activation of Cdc42 and RhoA was significantly increased, contributing to cell motility and phagocytosis. Additionally, the number of apoptotic cells was reduced in kif15 morphants, suggesting that Kif15 depletion could activate immune cells and efficiently remove apoptotic cells. Our study provides in vivo evidence that Kif15 is involved in immune cell migration and phagocytosis and suggests potential therapeutic roles for Kif15 inhibitors in spinal cord injury treatment.