Fig. 6

α9 integrin-kindlin-1 axons regenerate through laminin-111 isoform and tenascin-C-positive tissue. Sagittal sections were stained for A Laminin, B V5, and C GFAP. D The bridge that develops over lesions is mostly derived from connective and/or meningeal tissue and is therefore GFAP-negative and laminin-positive. Tangled axons and axons crossing the lesion from α9-kindlin group are seen inside the connective tissue bridge. Scale bar: 200 μm. E The detailed image shows the bridge region with growing axons with morphology typical for regenerates, and in some cases also with endbulbs. Scale bar: 100 μm. F Axon growth in the α9-kindlin group through connective tissue strands that are tenascin-C stained. Many axons with a typical regenerated morphology are seen within the strands, then entering CNS tissue rostral to the lesion on the left. Scale bar: 200 μm. To further characterize the bridge of connective tissue, the sagittal sections were then stained for G GFAP, H collagen 1α1 (fibroblasts), I CS-56 (CSPGs), and J V5. K The merged channels show that the bridge is also CSPG-positive, but the spatial distribution differs from being dispersed in the spared tissue to being oriented in the bridge. This suggests that the linear distribution of CSPGs may provide a pathway for axon elongation and thus influence neurite guidance. Scale bar: 200 μm. L The detailed image shows the bridge region with growing axons from G–K. Scale bar: 100 μm