Fig. 5: Distal TEC-specific Atg7 deletion resulted in the accumulation of p62/SQSTM1 and damaged mitochondria and increased oxidative stress. | Cell Death & Disease

Fig. 5: Distal TEC-specific Atg7 deletion resulted in the accumulation of p62/SQSTM1 and damaged mitochondria and increased oxidative stress.

From: Autophagy attenuates tubulointerstital fibrosis through regulating transforming growth factor-β and NLRP3 inflammasome signaling pathway

Fig. 5

a Representative immunoblots and b densitometry of expression of p62. b Representative immunofluorescent staining of THP (red) and p62 (green). The accumulation of p62/SQSTM1 was abundantly increased in the obstructed kidneys of Atg7flox/flox;Ksp-Cre+ mice, which was co-localized with THP which is a targeted-autophagy-deficient tubular cells of Atg7flox/flox;Ksp-Cre+ mice. Scale bars, 50 μm. c Ultrastructural alterations in tubular epithelial cell-specific Atg7 deletion after UUO. Majority of mitochondria in tubular epithelial cells had elongated cylindrical shape with organized cristae in WT mice after UUO, whereas the accumulation of damaged mitochondria with spherical shape and cristolysis were observed in Atg7 KO mice. Scale bars, 2 μm. d Representative Immunostaining and quantification of expression of 8-OHdG. Scale bars, 100 μm. e 8-OHdG levels in MDCK cells treated with H2O2 with or without Tempol. f Ultrastructural changes in MDCK cells induced by H2O2 with or without Tempol using transmission electron microscopy. Scale bars, 2 μm

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