Research Paper Volume 13, Issue 6 pp 8421—8439

PGC-1α alleviates mitochondrial dysfunction via TFEB-mediated autophagy in cisplatin-induced acute kidney injury

PGC-1α activates autophagy by modulating TFEB. (A) The expression of the proteins P62 and LC3 was measured by western blotting in HK2 cells exposed to cisplatin (5 μM) in the presence or absence of HCQ (30 μM) for 48 h. (B) HK2 cells were exposed to cisplatin in the presence or absence of ZLN005 (10 μM) for 48 h, and the expression of the proteins TFEB, P62 and LC3was measured by western blotting. (C) HK2 cells treated with ZLN005 (10 μM) and p62 mRNA was measured by real-time PCR. (D) Representative images of the colocalization between LC3 and mitochondria. Data are provided as the mean ± SEM, n=3 independent experiments. *P

Figure 7. PGC-1α activates autophagy by modulating TFEB. (A) The expression of the proteins P62 and LC3 was measured by western blotting in HK2 cells exposed to cisplatin (5 μM) in the presence or absence of HCQ (30 μM) for 48 h. (B) HK2 cells were exposed to cisplatin in the presence or absence of ZLN005 (10 μM) for 48 h, and the expression of the proteins TFEB, P62 and LC3was measured by western blotting. (C) HK2 cells treated with ZLN005 (10 μM) and p62 mRNA was measured by real-time PCR. (D) Representative images of the colocalization between LC3 and mitochondria. Data are provided as the mean ± SEM, n=3 independent experiments. *P < 0.05, **P < 0.01 vs. Con; &P < 0.05, &&P < 0.01 vs. Cisp. (Con, control; Zln, ZLN005; Cisp, cisplatin; C+Z, cisplatin + ZLN005; HCQ, hydroxychloroquine; C+H, cisplatin + hydroxychloroquine).