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

Figure 4.

Figure 4.

AMPK controls autophagy in podocytes. (A) Representative sections from 2-week-old mice bearing podocyte-specific deletion of Rptor or Tsc1 and controls stained for phosphorylated acetyl-CoA carboxylase Ser79 (p-ACACA) in red and NPHS1 (green). (B) Western blot out of glomerular lysates obtained from 2-week-old mice (genotype as indicated) for PRKAA and ULK1 and respective phosphorylation sites. (C) Densitometry for p-PRKAA Thr172 obtained from 3 WT glomerular lysates and 3 glomerular lysates obtained from 2-week-old mice bearing a podocyte-specific deletion of Rptor or Tsc1, respectively (** ≤ 0.01, * ≤ 0.05). (D) Densitometry for p-ULK1 Ser757, p-ULK1 Ser555 and p-ULK1 Ser317 obtained from 3 WT glomerular lysates and 3 glomerular lysates obtained from 2-week-old mice bearing a podocyte-specific deletion of Rptor or Tsc1, respectively (** ≤ 0.01, * ≤ 0.05). (E) Western blot from primary podocytes treated with AICAR (1 mM) for the time indicated (12 h or 24 h) to assess the abundance of p-ULK1 Ser555, p-PRKAA Thr172 and p-RPS6 Ser235/236. (F-H) Densitometry from (E) (** ≤ 0.01, * ≤ 0.05)