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. Author manuscript; available in PMC: 2014 Jun 25.
Published in final edited form as: Neuroscience. 2013 Mar 19;241:89–99. doi: 10.1016/j.neuroscience.2013.03.010

Figure 5. Schematic model for the possible mechanisms of ephrin B2 in the spinal cord injury repair.

Figure 5

A: In wild type mice ephrin B2 on astrocytes interacts with EphB2 on fibroblasts, inducing astrogliosis following SCI. The proliferation of astrocytes causes deposition of CSPG within the glial scar. CSPG interactions with their receptors produce an inhibitory effect to axonal re-growth. Interactions between EphA4 on axonal stump and ephrin B2 on astrocytes may repel axonal re-growth away from the glial scar due to the repulsive nature of ephrin/Eph signaling. The interaction of ephrin B2 and EphA4 on adjacent astrocytes (or next to each other on the same astrocyte) at the lesion site may also play a role in affecting growth inhibition.

B: Deletion of ephrin B2 induces decreased astrogliosis and less CSPG deposition and mitigates the inhibitory effect exerted by astrogliosis and CSPG. It also weakens the axonal collapse induced by ephrin B2 /EphA4 repulsive signaling. This model is suggestive based on our data and others; further studies are needed to firmly establish the pathway.