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. 2010 Feb 3;30(5):1839–1855. doi: 10.1523/JNEUROSCI.4459-09.2010

Figure 5.

Figure 5.

BMPR1a signaling affects GFAP levels independent of the canonical SMAD signaling pathway. A, Western blots for GFAP protein in injured cords from WT and BMPR1a CKO mice at 6 d post-SCI. The blot was stripped and reprobed for GAPDH (loading control). B, Normalized transcript levels of BMP4 and BMP7 in cords from WT and BMPR1a CKO mice at 6 d post-SCI showing no significant difference between the groups. C, Western blot analysis for Phospho (Tyr) STAT3 and total STAT3 in injured cords from 2 sets of littermates of WT and BMPR1a CKO animals at 4 d post-SCI. Activated STAT3 is present in the BMPR1a CKO mice. D, Densitometric analysis of the individual littermate pairs showing a slight increase in the levels of phospho-STAT3 as normalized to total STAT3 in the cords from BMPR1a CKO animals. E, Confocal Z-stacks taken from WT and BMPR1a CKO injured spinal cords (6 d post-SCI) stained for Hoechst nuclear stain (blue), npSMAD (green) and GFAP(red). Defective reactive astrocytes in BMPR1a CKO mice still have robust npSMAD (arrows). Scale bar, 20 μm. F, Single confocal Z-sections (from the stacks shown in E) taken at higher magnification with orthogonal projections showing intact npSMAD staining in the BMPR1a CKO astrocytes.