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. Author manuscript; available in PMC: 2017 Sep 1.
Published in final edited form as: Neurobiol Dis. 2016 May 1;93:226–242. doi: 10.1016/j.nbd.2016.04.010

Figure 11. Hypothetical model by which activation of PAR1 may contribute to astrogliosis.

Figure 11

Thrombin and neurosin are increased in the spinal cord in the context of traumatic injury and activate astrocyte PAR1 to promote expression and secretion of IL- 6. IL-6 in turn activates STAT3 signaling and feeds back to increase the expression of PAR1 activators (thrombin and neurosin), driving the canonical IL-6-STAT3 signaling cascade and fulminant astrogliosis forward. While this simplified model suggests a mechanism for PAR1 signaling in driving astrogliosis after SCI it does not exclude PAR1 signaling in neurons, myelinating cells and microglia as additional significant contributors to SCI pathogenesis.