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. Author manuscript; available in PMC: 2012 Oct 1.
Published in final edited form as: Lab Invest. 2012 Feb 13;92(4):532–542. doi: 10.1038/labinvest.2012.6

Figure 4. E2-induced vessel growth in injured nerves requires Shh-pathway activation.

Figure 4

(A–C) Ptch1-LacZ mice were injected with saline (placebo); with E2 (100 μg administered 1 week before sciatic nerve-crush injury); with cyclopamine (CYC) (50 mg/kg per day from 2 days before nerve-crush injury until sacrifice), which blocks hedgehog signaling by interfering with smo; or with both E2 and cyclopamine. (A) Functional vasculature was identified in sections of injured nerve tissue by injecting mice with fluorescein-conjugated BS-1 lectin 15 minutes before sacrifice on day 28 after injury. (B) Capillary density was evaluated by staining cross sections of the vasa nervorum from mice sacrificed on day 28 with the endothelial-cell marker CD31 and quantified. *P<0.01 versus placebo, CYC, or E2+CYC. (C) Ptch1 protein expression was evaluated in X-gal–stained whole-mount tissues from injured nerves, quantified, and presented as a percentage of the whole-nerve area. *P<0.05 versus placebo, CYC, or E2+CYC. (D) Gli1-LacZ mice were injected with saline (placebo), E2, cyclopamine, or both E2 and cyclopamine and sacrificed 28 days after sciatic nerve-crush injury; then, Gli1 protein expression was evaluated in X-gal–stained whole-mount tissues from the injured nerve, quantified, and presented as a percentage of the whole-nerve area. *P<0.05 versus placebo, CYC, or E2+CYC.