Fig. 5: In neonatal lungs AMPK-α1/α2 deletion has no effect on alveolar number or wall thickness but increases medial thickness of pulmonary arteries.

Representative images of alveoli in lung slices from non-terminal samples stained for α-smooth muscle actin from (a) age-matched AMPK-α1/α2 floxed (AMPK-α1/α2 FLX) controls and (b) AMPK-α1/α2 KOs. Scatter plots show (c) alveolar number per mm2 (n = 5 mice per genotype, averaged from 2 mm2 area per mouse), (d) alveolar wall thickness (n = 5 mice per genotype, averaged from 70–90 septa per mouse) and (e) medial thickness of pulmonary arteries for non-terminal samples of AMPK-α1/α2 KO (orange, n = 5 mice, n = 4 fields, averaged from 16–25 arteries per mouse) vs age-matched AMPK-α1/α2 FLX (gray, n = 5 mice, n = 4 fields, averaged from 16-22 arteries per mouse). Data are expressed as mean ± SEM. Statistical significance was assessed by two-sided unpaired Mann–Whitney’s test.