Fig. 6: Conditional deletion of Lkb1 and AMPK in tyrosine hydroxylase expressing cells attenuates increases in breathing frequency during hypoxia but only Lkb1 deletion augments increases in tidal volume during severe hypoxia.
From: LKB1 is the gatekeeper of carotid body chemosensing and the hypoxic ventilatory response
Dot plots of mean ± SEM for changes in a breathing frequency and b tidal volume at the peak of the Augmenting Phase (~30 s), at ~100 s following Roll Off and during the plateau of the Sustained Phase (~300 s) of the ventilatory response to mild (12% O2) and severe (8% O2) hypoxia for TH-Cre (black; 12% O2, n = 25 independent experiments; 8% O2, n = 37 independent experiments), Lkb1 homozygous floxed (Lkb1 hom Fx, blue; 12% O2, n = 14 independent experiments; 8% O2, n = 15 independent experiments) that are ~90% hypomorphic for LKB1 and conditional Lkb1 homozygous knockout mice (Lkb1 hom KO, red; 12% O2, n = 22 independent experiments; 8% O2, n = 30 independent experiments). These data are also compared with outcomes for AMPKα1 + α2 homozygous floxed mice (AMPKα1 + α2 hom Fx, beige, 12% O2, n = 30 independent experiments; 8% O2, n = 13 independent experiments) and conditional AMPKα1 + α2 homozygous knockout mice (AMPKα1 + α2 hom KO, purple, 12% O2, n = 30 independent experiments; 8% O2, n = 26 independent experiments). *=p < 0.05, **=p < 0.01, ****=p < 0.0001 compared to TH-Cre.
