Skip to main content
. 2017 Aug 4;6(8):e005506. doi: 10.1161/JAHA.117.005506

Figure 1.

Figure 1

Efficient inhibition of mTORC1 in neonatal mice by rapamycin treatment of pregnant dams. A, Western blots of protein extracts from neonatal (P1) heart, kidney, and lung tissue after prenatal vehicle or rapamycin treatment. Reduced phosphorylation of the mTORC1 downstream targets S6K1 and S6 ribosomal protein confirmed successful mTORC1 inhibition by rapamycin in all 3 organs. In contrast, phosphorylation of 4E‐BP1 was unaffected in the neonatal heart. B, Western blots revealed reduced p62 (SQSTM1) and LC3B‐I protein levels, resulting in an increased LC3B‐II/LC3B‐I ratio in hearts of rapamycin‐ compared to vehicle‐treated neonates (densitometric quantification n=6 per group for p62, n=4 for LC3B, *P<0.05, **P<0.01). C, Western blots of Akt Ser473 phosphorylation normalized to total Akt revealed no significant differences between hearts of rapamycin‐ and vehicle‐treated neonates (densitometric quantification n=5 per group). D, Western blots of heart protein extracts from vehicle‐treated neonates at P1 and rapamycin‐treated littermates at P1, P2, and P3 illustrating phosphorylation status of S6 ribosomal protein. mTORC1 activity is still inhibited at P2 but restored by P3. B and C, Samples were detected on the same membrane but were noncontiguous, indicated by a black line.