Pten controls lung morphogenesis, bronchioalveolar stem cells, and onset of lung adenocarcinomas in mice
J. Clin. Invest. Shigehisa Yanagi, et al. 117:2929 doi:10.1172/JCI31854 [Go to this article.]

Figure 1
Abnormal lung morphogenesis and lung epithelial cell hyperplasia in SOPten^flox/flox(E10–E16) mice. (A) Gross appearance of representative neonates. Skin color is normal in WT(E10–E16) neonates but cyanotic in SOPten^flox/flox(E10–E16) (KO) littermates. (B) Histologic analysis of neonatal lungs. Left: normal alveolar (Al) and bronchiolar (Br) epithelial cells from a WT(E10–E16) neonate. Right: epithelial cell hyperplasia in alveoli and a bronchiole from a SOPten^flox/flox(E10–E16) neonate. Scale bars: 50 μm. (C) Increased total cell numbers in lungs. Total cells from WT(E10–E16) and SOPten^flox/flox(E10–E16) lungs at P0 were counted. Data are expressed as the mean total lung cells ± SD for 4 mice/group. *P < 0.05, Student’s t test. (D) Histological analysis of lungs at various embryonic stages. Lung sections were prepared from SOPten^flox/flox(E10–E16) mice at the indicated gestational stages and stained with H&E. Representative sections from WT(E10–E16) and SOPten^flox/flox(E10–E16) embryos are shown. No differences were detected between the WT and mutant embryos at E14.5 or E16.6, but dramatic differences were visible from E17.5 onward. WT(E10–E16) lungs showed dilatation of distal tubules and mesenchyme thinning at E17.5, with progression of septation from E17.5 to P0. SOPten^flox/flox(E10–E16) lungs showed fewer saccular structures during this period. Scale bars: 200 μm.