Fig. 8: Knockdown of RIPK1 further decreases the Hsp90 levels in the cytoplasm and increases the translocation of Hsf1 from the cytoplasm to the nucleus in the ischemic cerebral cortex or in OGD-treated astrocytes. | Acta Pharmacologica Sinica

Fig. 8: Knockdown of RIPK1 further decreases the Hsp90 levels in the cytoplasm and increases the translocation of Hsf1 from the cytoplasm to the nucleus in the ischemic cerebral cortex or in OGD-treated astrocytes.

From: RIPK1 inhibition contributes to lysosomal membrane stabilization in ischemic astrocytes via a lysosomal Hsp70.1B-dependent mechanism

Fig. 8

a, c Knockdown of RIPK1 decreases the Hsp90 levels in the cytoplasm and increases the translocation of Hsf1 from the cytoplasm to the nucleus in the ischemic cerebral cortex. a Representative photomicrographs of double immunohistochemistry staining for Hsp90 and Hsf1 in the ischemic cerebral cortex (Hsf1: red; Hp90: green; Hoechst: blue). Scale bars indicate 10 μm. c Quantitative analysis of Hsp90/Hsf1 fluorescence intensity in a. Manders’ overlap coefficient demonstrates the colocalization between Hsp90 and Hsf1, as well as that between Hsf1 and Hoechst. Means ± SDs, n = 6. **P < 0.01. b, d Knockdown of RIPK1 decreases the Hsp90 levels in the cytoplasm and increases the translocation of Hsf1 from the cytoplasm to the nucleus in OGD-treated astrocytes. b Representative photomicrographs of double immunostaining of Hsp90 and Hsf1 in astrocytes (Hsf1: red; Hsp90: green; Hoechst: blue). Scale bars indicate 50 μm. Magnified images are cropped sections from the areas indicated with white borders. Scale bars indicate 10 μm. d Quantitative analysis of Hsp90/Hsf1 fluorescence intensity in b. Manders’ overlap coefficient demonstrates the colocalization between Hsp90 and Hsf1 as well as that between Hsf1 and Hoechst. Means ± SDs, n = 6. **P < 0.01. Statistical analysis was performed with one-way ANOVA followed by a post hoc Tukey test.

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