Skip to main content
. 2013 Mar 8;123(4):1705–1717. doi: 10.1172/JCI64149

Figure 9. Flow chart shows how GSK3β signaling cooperates with CXCL12/CXCR4 signaling in murine HSPCs by governing their preferential and directional motility.

Figure 9

At ZT5, GSK3β expression is at its peak as is the number of circulating HSPCs, whereas at ZT13, GSK3β expression is at its lowest point, as is the number of circulating HSPCs. GSK3β inhibition by BIO-A rapidly impairs HSPC steady-state egress and migratory potential. NE induces rapid mobilization of HSPCs and enhances their motility, demonstrating upregulated GSK3β expression. IGF-1 administration for 1 week limits the egress of HSPCs and reduces their motility, demonstrating downregulated GSK3β expression. PQ401, which is an IGF-1R antagonist, induces rapid HSPC mobilization in a GSK3β-dependent manner. In vitro SCF treatment enhances HSPC migratory capacity, demonstrating upregulated GSK3β expression. GSK3β signaling thereby promotes HSPC motility by controlling the rearrangement of cytoskeletal machinery (i.e., control over actin and MT dynamics). Short-term denotes hours; long-term denotes days.