Skip to main content
Figure 2 | Journal of Neuroinflammation

Figure 2

From: Microglial TIR-domain-containing adapter-inducing interferon-β (TRIF) deficiency promotes retinal ganglion cell survival and axon regeneration via nuclear factor-κB

Figure 2

TIR-domain-containing adapter-inducing interferon-β deletion promotes optic nerve regeneration. (A) Longitudinal sections through an optic nerve immunostained to detect growth-associated protein43-positive axons distal to the injury site (*) at 0, 1, 3, 7 and 28 days after nerve crush. The trif -/- mice exerted more robust regeneration ability than the wild-type (WT) mice. In WT mice, few axons were regenerated beyond the lesion site (*), in contrast to the trif -/- group, in which regeneration was particularly marked at 28 days post-crush (28dPC). Upper scale bar = 100 μm, bottom scale bar = 50 μm. (B) Estimated number of regenerated fibers (> 100, 200, 300, 400, and 500 μm from the lesion site) at 3dPC and (C) 7dPC in the WT and trif -/- groups. *P < 0.05, **P < 0.01, increase relative to WT. (D) Quantification of outgrown axons of in vitro retinal ganglion cells (RGCs) by GAP43 immunostaining. Axon length was calculated by two observers using a double-blinded method, under a microscope. Mean length of axons was measured using a micrometer.

Back to article page