Figure 9.

Model showing the opposing effects of BMPR1a and BMPR1b signaling after spinal cord injury. Schematic representation of the effects of BMPR1a and BMPR1b signaling on reactive gliosis in the acutely injured spinal cord. SCI causes an upregulation of BMPR1a in reactive astrocytes (blue arrow in top row) in the WT cord, which promotes reactive astrocytic hypertrophy and limits infiltration by inflammatory cells (green ovals). BMPR1b signaling negatively regulates this process. In the absence of BMPR1a signaling, the balance shifts toward BMPR1b (dotted lines in the middle panel), which causes defective astrocytic hypertrophy and increased infiltration in the BMPR1a CKO animals. In contrast, in the BMPR1b KO mice, there is more pronounced BMPR1a signaling (dotted blue arrows) which causes a smaller lesion size with greater compaction of the inflammatory cells.