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. 2015 Jun 24;35(12):1937–1949. doi: 10.1038/jcbfm.2015.150

Figure 1.

Figure 1

CDK5miR prevents CDK5 and calpain activities in ischemic rats at 1 month after ischemia. (A) CDK5 expression in CA1 (bregma −2.56). (a) Green fluorescent protein (GFP) represents the transduced CA1 cells in the contralateral and ipsilateral hemispheres. (b) The sections were photographed at × 10 and × 40, scale bars=50 μm ( × 10) and 25 μm ( × 40). The animals were killed 1 month after CDK5miR or SCRmiR were unilaterally injected into the right CA1 region. (c) Quantification of the fluorescence intensity of CDK5 immunoreactivity of transduced neurons using the software image Scope-Pro from Media Cybernetics. n=4 to 6, *P<0.05; **P<0.001. (B) The ipsilateral CA1 was dissected, and CDK5 kinase activity was detected using a phosphorylated histone antibody. A band corresponding to the IgG heavy chain was detected. Densitometric quantification was performed. pHISTONE was relativized respect to the total CDK5 from lysates, relativized to the loading control (tubulin). n=4 to 6, **P<0.001. (C) (a) CDK5, (b) p35, and (d) CDK5 protein levels from the CA1 regions of animals treated with SCRmiR and CDK5miR. Representative bands from western blotting are shown. (c) The p25/p35 ratio was established. Densitometric quantification was relativized to the loading control (tubulin) and normalized to the internal control (SCRmiR-treated sham rats). The values are mean±s.e.m. (D) Calpain activity was measured in the ipsilateral CA1 region. n=4 to 6, *P<0.05, ***P<0.0001. CDK5, cyclin-dependent kinase 5; RU, relative units; SCR, scrambled RNA sequence.