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. 2017 Aug 31;76(10):898–907. doi: 10.1093/jnen/nlx074

FIGURE 2.

FIGURE 2

Upregulation of αEnsa protein in rat tMCAo is detected using a monoclonal mouse-anti-αEnsa primary antibody. Double label immunofluorescence reveals prominent upregulation of αEnsa protein in NeuN-positive neurons (A), GFAP-positive astrocytes (C) and PECAM (CD31)-positive endothelial cells (E) in ischemic tissues, versus nonischemic contralateral controls (B, D, and F, respectively); merged double label images are shown in the third and fourth columns; original magnification, 40× (A–F); scale bars, 10 µm; αEnsa, red/CY3; NeuN, GFAP, and PECAM (CD31), green/FITC; nuclei, blue/DAPI. Images shown are from specimens 24 hours after ischemia/reperfusion. Immunoblot of αEnsa and Hsc70 protein expression in control versus peri-infarct region following 2 hours ischemia and 4 hours reperfusion in rat MCAo (data shown from 2 controls and 2 animals with tMCAo, representatiave of 6 independent experiments); molecular weight ladder in lane 5 and human recombinant αEnsa (positive control) in lane 6 (G).