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. 2019 Dec 23;16(11):1932–1948. doi: 10.1080/15548627.2019.1705007

Figure 5.

Figure 5.

Activation of AMPK stimulates autophagy independently of MTORC1 activity. (A) Western blot from Tsc1-deficient podocytes and corresponding WT controls with and without AICAR treatment (1 mM, 24 h) to assess the abundance of phosphorylated forms of ULK1 and PRKAA as indicated. (B) Densitometry from (A) (** ≤ 0.01, * ≤ 0.05). (C) Representative section from 2-week-old mice bearing podocyte-specific deletion of Rptor with and without AICAR treatment (500 mg/kg BW 24 h and 4 h before harvest) stained with LC3 (red) and NPHS1/nephrin in green. (D) Representative section from 2-week-old mice bearing podocyte-specific deletion of Rptor with and without AICAR treatment (500 mg/kg BW 24 h and 4 h before harvest) stained with SQSTM1 (red) and NPHS1/nephrin in green. (E) Quantification of LC3 puncta per glomerular area (n = 3 each, 30 glomeruli counted per mouse, * ≤ 0.05). (F) Quantification of SQSTM1 puncta per glomerular area (n = 3 each, 30 glomeruli counted per mouse, * ≤ 0.05). (G) Western blot from glomerular lysates from 2-week-old mice bearing podocyte-specific deletion of Rptor with and without AICAR treatment (500 mg/kg BW 24 h and 4 h before harvest) to assess the abundance of LC3-II. (H) Densitometry from (G) (* ≤ 0.05)