Fig. 6.

Reducing BMP4 signaling activity rescued atelectasis phenotype of Fstl1^−/− embryonic lung explants. (A) Noggin increased saccular dilation of Fstl1^−/− fetal lung explants. E15.5 lung explants from WT and Fstl1^−/− littermates were cultured for 48 to 54 h in absence (CTL) or presence of Noggin (500 ng/mL). H&E staining of explant sections shown at low (Upper) and high (Lower) magnification. Saccular dilation was shown in Noggin treated-Fstl1^−/− explants. The percentage of the total examined sac area of the lung section is shown in the top right corner of each diagram (Upper). (Scale bar, 100 μm.) (B) Fstl1 (100 ng/mL) inhibited BMP4-increased SFTPC expression in A549 cells. The data represent the mean ± SEM of three independent experiments. (C) Summary of the role of Fstl1 in embryonic lung development. Fstl1 modulates BMP4-induced Smad-1/5/8 activity and inhibits pro–SP-C expression.