Skip to main content
. 2018 Sep 20;3(18):e99592. doi: 10.1172/jci.insight.99592

Figure 7. Becn1+/– mice have decreased mitophagy at baseline that does not increase after cigarette smoke exposure.

Figure 7

(A) Mitochondria of renal tubular epithelial cells of WT mice exposed to cigarette smoke (CS), showing invaginations (arrow) and loss of mitochondrial matrix (arrowhead) relative to RA control. Scale bars: 500 nm (top) and 200 nm (bottom). (B) Quantification of LC3B detected in mitochondrial fractions from WT mice, normalized to TOM20 and room air (RA) control (n = 9 for RA, n =10 for CS). (C) Representative Western blot of NDP52 in mitochondrial fractions from WT mice exposed to 6 months of CS compared with RA. Graph represents quantification of Western data normalized to TOM20 and RA control (n = 9 for RA, n = 10 for CS). (D) Quantification of Western blots of LC3B, NDP52, Parkin and (E) Mitochondrial transcription factor A (TFAM) expression detected in mitochondrial fractions after 6 months of CS or RA exposure in Becn1+/– mice relative to Becn1+/+ mice. Data were normalized to TOM20 and control (n = 10/group for Becn1+/+ mice, and n = 4/group for Becn1+/– mice). All data are mean ± SEM. *P < 0.05, **P < 0.01, analyzed by Student’s t test (B and C) and 1-way ANOVA with Bonferroni’s post hoc test (D and E). (F) Diagram representing CS-induced kidney injury. After systemic exposure to CS, autophagy is upregulated in kidneys in association with kidney injury. Becn1+/– mice have reduced autophagy and display reduced kidney injury after CS exposure. The increased autophagic activity and autophagosome turnover in response to CS exposure reduces Beclin-1 steady-state levels, as a potential compensatory mechanism.