Figure 7.

BMPR1b knock-out mice have increased GFAP levels and reduced lesion volumes in acute stages following injury, but a reduced glial scar in chronic stages following injury. A, Low-magnification (10×) montages of WT and BMPR1b KO mouse spinal cords at 1 week postinjury, stained with Hoechst nuclear stain(blue), CD11b (green) and GFAP (red). The reactive gliosis at the edge of the lesion appears similar in WT and KO mice. However, the area compacted between the wall of reactive astrocytes is smaller in the KO. CD11b-positive cells have already been largely compacted into this area while this region continues to be mostly acellular in the WT mice as evidenced by the Hoechst stain. Scale bar, 200 μm. B, Spinal cord sections stained for myelin and cresyl violet showing smaller lesion size in BMPR1b KO mice. Scale bar, 250 μm. C, Western blot for GFAP from total protein extracted from injured spinal cords at 6 d postinjury from WT and BMPR1b KO animals. D, WT and BMPR1b KO spinal cords at 5 weeks postinjury, stained with Hoechst nuclear stain (blue) and GFAP (red). The GFAP-positive astrocytes have walled off the inflammatory cells but there are fewer astrocytes in the area adjacent to them. (Scale bar: 200 μm). E, Higher-magnification images of the area adjacent to the lesion (in D) showing reduced gliosis in the BMPR1b KO mice. Scale bar, 100 μm. F, Quantification of the GFAP-negative lesion area in WT and BMPR1b KO mice at 1 and 5 weeks postinjury.