HDAC6 Regulates the Chaperone-Mediated Autophagy to Prevent Oxidative Damage in Injured Neurons after Experimental Spinal Cord Injury

Figure 4

Loss of HDAC6 leads to the hypersensitivity to HI-induced stress. The PC12 and PC12/siHDAC6 cells were treated with HI for 24 h. Ctrl express vehicle-treated group. (a) Apoptotic cells were calculated by flow cytometry with simultaneous staining of annexin V-FITC and PI. (b) The ultrastructural features of PC12 cells in different groups. In control cells (A) and HDAC6-deficient cells (C), the nucleoplasm (thin arrows) remained condensed and all kinds of organelles scattered within the cytoplasm (thick arrows and triangles). HI treatment induced autophagy (B); the lysosome amplification and autophagy bubbles appear in the cytoplasm (asterisks). (D) Knockdown of HDAC6 elicited apoptotic features in cells exposure to HI. Cell swelling, cytoplasmic vacuolization (triangles), and nuclear chromatin loss and margination (thin arrows). Scale bar: 1 μm.

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