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. 2001 Sep 15;15(18):2421–2432. doi: 10.1101/gad.922801

Figure 7.

Figure 7

Figure 7

JIP1 deficiency causes reduced oxygen and glucose deprivation-induced JNK activation and apoptosis of hippocampal neurons. (A,B) Wild-type (A) and Jip1−/− (B) hippocampal neurons were cultured in vitro and visualized by MAP2 immunocytochemistry. (C,D) Activated JNK (red) was detected by immunofluorescence analysis of wild-type (C) and Jip1−/− (D) hippocampal neurons following oxygen and glucose deprivation (OGD) challenge (4 h) and recovery (12 h) by staining with an antibody to phospho-(pThr183pTyr185)-JNK. Neurites were detected by staining with an antibody to MAP2 (green). A marked increase in the amount of activated JNK was observed in wild-type neurons (C), but not in Jip1−/− neurons (D) following exposure to stress. (E,F) Cell death was measured by the percentage of TUNEL-positive nuclei (red) in the total number of bis-benzimide-stained nuclei (blue) following OGD challenge (4 h) and recovery (24 h). Increased numbers of apoptotic neurons were detected in wild-type (E) compared with Jip1−/− (F) cultures. (G,H) The survival of wild-type (G) and Jip1−/− (H) hippocampal neurons was compared by MAP2 immunocytochemistry following OGD challenge (4 h) and recovery (48 h). (I,J) Wild-type and Jip1−/− hippocampal neurons were exposed to OGD challenge. Apoptosis measured by TUNEL assay (I) and survival measured by MAP2 staining (J) was quantitated in three independent experiments (mean ± SD). Scale bar in H, 200 μm (panels A,B,EH) and 20 μm (panels C,D).

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