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. Author manuscript; available in PMC: 2013 Jan 1.
Published in final edited form as: Neurobiol Dis. 2011 Sep 24;45(1):555–563. doi: 10.1016/j.nbd.2011.09.012

Fig. 5.

Fig. 5

Effect of miR-181 up- or down-regulation on miR-181a, GRP78, and infarction after focal ischemia. A. Mice injected ICV with pri-miR-181ab plasmid show elevated brain levels of miR-181a by RT-qPCR. B. Mice pretreated with miR-181a antagomir show reduced levels of miR-181a in the brain. C. GRP78 protein levels are decreased in the brains of mice pretreated with pri-miR-181ab plasmid. D. GRP78 protein levels increased in brains pretreated with miR-181a antagomir. Representative immunoblots are shown under the graphs. N=4 mice in each group for A to D. E. Representative cresyl violet-stained coronal sections demonstrate an increased infarct size in a representative miR-181a overexpressing brain compared with the brain of a miR-181 seed mutation (SM)-injected animal also subjected to MCAO. F. The bar graph shows quantitation of infarct size by cresyl violet staining for the group of mice. G. Representative cresyl violet stained brains of miR-181a antagomir transfected or mismatch (MM) miR-181a-antagomir-injected animals. H: The graph shows quantification of the infarct size. N=7 mice/group for E to H. *P<0.01 compared to SM or MM control by T-test.