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. 2012 Apr 23;109(19):7505–7510. doi: 10.1073/pnas.1121146109

Fig. 2.

Fig. 2.

Up-regulation of HMGB1 in reactive astrocytes in the peri-infarct cortex after transient focal ischemia in mice. (A) GFAP+ reactive astrocytes accumulate in the peri-infarct cortex by 14 d poststroke. (Magnification, 10×.) (B) Western blots of brain homogenates show elevation of HMGB1 and its associated nuclear export protein CRM1 in the peri-infarct cortex at 14 d poststroke. (C) Densitometric quantitation of HMGB1 and CRM1 at day 14 compared with day 3 after stroke. #P < 0.05 vs. day 3. (D and E) Immunostaining demonstrates colocalization of both HMGB1 and its nuclear export protein CRM1 in GFAP+ reactive astrocytes within the peri-infarct cortex.