Figure 8.
Schematic diagram of the present study. After subarachnoid hemorrhage (SAH), elevated nexilin levels facilitate F-actin rearrangement and then promote oligodendrocyte progenitor cell (OPC) migration and remyelination. Nexilin expression is negatively regulated by the activated thrombin receptor protease-activated receptor 1 (PAR1) on the OPC membrane, which is followed by the activation of downstream Ras-proximate-1 (RAP1) and the promotion of RAP1 phosphorylation. The suppression of PAR1 by thrombin receptor antagonist peptide (TRAP) inhibits PAR1 signaling but enhances nexilin and promotes OPC migration and remyelination after SAH.