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. 2009 Feb;174(2):586–594. doi: 10.2353/ajpath.2009.080661

Figure 1.

Figure 1

TPA mediates cerebral ischemia-induced microglial activation via a plasminogen-independent mechanism. A: Representative micrographs corresponding to immunohistochemical analysis of microglial activation in the AOI-2 24 hours after transient middle cerebral artery occlusion (tMCAO) in wild-type (a–d), and tPA−/− (e–h) mice, as well as in tPA−/− mice treated with tPA (i–l), and in Plg−/− mice (m–p). c, g, k, and o represent the merged images corresponding to the ipsilateral, ischemic hemisphere, whereas d, h, l, and p are the merged images for the corresponding area in the contralateral, nonischemic hemisphere. Blue is DAPI, red is F4/80, and green is β-isolectin. The insets in a–c correspond to a higher magnification of examples of cells with ameboid morphology and positive for β-isolectin and F4/80. Images were visualized using a Leica DMRBE microscope (Leica, Houston, TX) equipped with a 100×/1.30 numerical aperture (NA) and a LeicaDC500 camera. B: Average percentage of active microglial cells in each AOI 24 hours after tMCAO in wild-type (Wt, white bars), tPA−/− (black bars), and Plg−/− (gray bar) mice. atPA denotes treatment with active tPA whereas itPA denotes treatment with inactive tPA immediately after tMCAO. NT, no treatment. n = 10. Bars indicate SEM. NS, nonsignificant. Original magnifications: ×20 (a–p); ×40 (insets in a–c).