Fig. 5: Deficiency of ATG7-dependent autophagy promotes reactive oxygen species (ROS) generation and activation of the Nrf2-ARE signaling pathway in NHEM under oxidative stress, whereas enhancement of autophagy protects NHEM against oxidative stress. | Cell Death Discovery

Fig. 5: Deficiency of ATG7-dependent autophagy promotes reactive oxygen species (ROS) generation and activation of the Nrf2-ARE signaling pathway in NHEM under oxidative stress, whereas enhancement of autophagy protects NHEM against oxidative stress.

From: Dysfunction of ATG7-dependent autophagy dysregulates the antioxidant response and contributes to oxidative stress-induced biological impairments in human epidermal melanocytes

Fig. 5

a NHEM transfected with control shRNA, ATG7 shRNA, empty vector, or lentivirus ATG7 were treated with H2O2 (200 μM) for 24 h or UVB irradiation (12 mW/cm2) for 60 s. Intracellular reactive oxygen species (ROS) levels were measured by flow cytometry assay. Relative quantification of intracellular ROS levels was analyzed in transfected NHEM treated with or without H2O2 or UVB. b Relative mRNA expression of GCLC, p62, GCLM, NQO-1, HO-1, and GSTM-1 in NHEM transfected with control shRNA or ATG7 shRNA. c Representative images of western blotting and statistical analysis of western blotting data of GCLC, p62, GCLM, NQO-1, HO-1, and GSTM-1 in NHEM transfected with control shRNA or ATG7 shRNA. GAPDH was used as a protein loading control. Data are presented as mean ± SD, n = 3. *P < 0.05, **P < 0.01. d Relative mRNA expression of GCLC, p62, GCLM, NQO-1, HO-1, and GSTM-1 in NHEM transfected with empty vector or lentivirus ATG7. e Representative images of western blotting and statistical analysis of western blotting data of GCLC, p62, GCLM, NQO-1, HO-1, and GSTM-1 in NHEM transfected with empty vector or lentivirus ATG7. GAPDH was used as a protein loading control. Data are presented as mean ± SD, n = 3. *P < 0.05, **P < 0.01, ns, nonsignificant.

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