神经损伤与修复
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Figure 1 ｜ Schematic drawing visualizing the improved axonal regeneration caused by CXCR4- or CXCL12-knockout.
To confirm the CXCL12 secretion from axons’ tips, in vitro experiments were done with virally transduced sensory neurons to overexpress CXCL12, which were then seeded into special chambers that physically separated the cell bodies from their axonal tips. Using ELISA, it was possible to detect secreted CXCL12, but not when applying the protein-secretion inhibitor, proving that axons can release CXCL12. Moreover, an HA-tagged version of CXCL12 was virally expressed in RGCs. Interestingly, after ONC, the HA signal accumulated in fibers at the lesion site and diffusely around the growth cones (Hilla et al., 2021), providing more evidence of its secretion into the injury site (Figure 1).