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Fig. 1 | Translational Neurodegeneration

Fig. 1

From: Suppression of astrocytic autophagy by αB-crystallin contributes to α-synuclein inclusion formation

Fig. 1

CRYAB regulates autophagy process in vitro. a Knockdown of CRYAB enhances the conversion of LC3-I to LC3-II in U251 cells. U251 cells were transfected with CRYAB siRNA (siNC: the siRNA of negative control; siCRYAB: the siRNA of CRYAB) and the cellular LC3 levels were assessed by Western blotting 48 h after transfection. Data are presented as mean ± SEM, n = 6. Unpaired t-test. **P < 0.01. b Overexpression of CRYAB inhibits LC3-II formation in U251 cells. The cellular LC3 levels were assessed by western blotting 48 h after transfection. Data are presented as the mean ± SEM, n = 3. Unpaired t-test. **P < 0.01. c CRYAB overexpression in primary astrocytes inhibits LC3-II formation. Primary cultured astrocytes were transfected with lentivirus vector encoding CRYAB. The cellular LC3 levels were assessed by Western blotting 48 h after transfection. Data are presented as mean ± SEM, n = 3. Paired t-test. *P < 0.05. d U251 cells were transfected with siCRYAB in the presence or absence of H2O2 (1 mM, 6 h). The cellular p62 levels were assessed 48 h after transfection using western blotting. Data are presented as mean ± SEM, n = 3. *P < 0.05. e Knockdown of CRYAB leads to a marked increase in the number of autophagic vacuoles. Autophagic vacuoles in U251 cells transfected with siNC or siCRYAB were examined using electron microscopy. The arrows indicate autophagic vacuoles. Scale bars: 0.5 μm. The graph shows a statistical analysis of cytoplasmic occupancy of autophagic vacuoles in the cells. Data are presented as mean ± SEM. Twenty cells in each group were examined. Unpaired t-test. ***P < 0.001

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