Figure 2.

Fasudil activity in the spinal cord is Smn-independent and does not prevent motor neuron loss in the ventral horn region. (A and B) Spinal cords were obtained from post-natal (P) day 21 untreated wild type (WT), vehicle-treated Smn2B/- and fasudil-treated Smn2B/- mice. (A) Immunoblot analysis shows that spinal cords treated with the rho-kinase (ROCK) inhibitor fasudil have decreased levels of p-cofilin, a known substrate of ROCK. (B) Immunoblot analysis shows that fasudil does not increase Smn protein levels in the spinal cords of Smn2B/- mice. (C and D) Spinal cord sections were analyzed from P21 untreated wild type (WT) (n = 3), vehicle-treated Smn2B/- (n = 3) and fasudil-treated Smn2B/- (n = 3) mice. (C) Representative images of hematoxylin and esoin (H&E)- and HB9-stained spinal cord sections. Arrowhead depicts a typical large motor neuron. Scale bar = 50 μm. (D) Quantification of motor neurons within the ventral horn region of the spinal cord shows that fasudil does not prevent the motor neuron loss that occurs in vehicle-treated Smn2B/- mice (*P < 0.05; **P < 0.01; NS = not significant; data are mean +/- s.d.).

Bowerman et al. BMC Medicine 2012 10:24   doi:10.1186/1741-7015-10-24
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