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. 2017 Nov 6;2017:6818970. doi: 10.1155/2017/6818970

Figure 2.

Figure 2

S1PR1 knockdown potentiates CNTF-induced axonal regeneration. (a) Axonal regeneration was visualized on longitudinal sections of optic nerves two weeks after crush injury and 4 weeks after coinfection with ShH10.CNTF and AAV2 vectors. Axons were traced with cholera toxin β subunit (CTb) conjugated to Alexa 594 the day before tissue fixation. (b) The infection of retinal cells with ShH10.CNTF and AAV2.shRNA-S1PR1 promoted lengthy axonal regeneration in the optic nerve compared with the ShH10.CNTF/AAV2.GFP combination. (c) Quantitatively, axonal fibers were significantly more numerous between 1300 and 1800 μm past the lesion site with ShH10.CNTF/AAV2.shRNA-S1PR1 (n = 6 mice) than with ShH10.CNTF/AAV2.GFP (n = 5 mice) treatments (ANOVA, ∗p < 0.05). ShH10.CNTF/AAV2.S1PR1 did not influence axonal regeneration (n = 6 mice). (d) The measurement of the longest axons revealed better growth distances in ShH10.CNTF-/AAV2.shRNA-S1PR1-treated animals than in mice receiving ShH10.CNTF/AAV2.GFP. Scale bars: (b) top = 200 μm; (b) bottom = 100 μm.