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Fig. 2. Expression of Tgfbi, a target of the Tgfß pathway,
under RA-sufficient and -deficient conditions. (A-C) X-Gal staining
of E9.5 RARElacZ mouse embryo showing strong signals in the foregut
region (A, between the dashed lines), where Tgfbi expression is
minimal by WMISH (asterisk in B,C, between dashed lines). By contrast,
Tgfbi signals are significantly stronger in the same region of the
Raldh2-/- foregut in vivo (C, arrowhead), compared with a
WT littermate. (D) WMISH showing high levels of expression of
Tgfbi in a non-RA-supplemented Raldh2-/- foregut
explant. The Tgfbi expression domain depicted in the boxed area
includes the thyroid (Th) and the region where the lung failed to form.
(E) WMISH of Nkx2.1 in Raldh2-/- control
cultures. Asterisk (in the enhanced-contrast image of the explant, D, right;
E) marks the presumptive lung field. (F,G) Tgfbi
expression is dramatically reduced in Raldh2-/- foregut in
which lung (Lu) bud formation was rescued by RA supplementation (F,
arrowhead). H&E staining of paraffin-embedded section of RA-supplemented
Raldh2-/- reveals bud formation in the presumptive lung
region of the foregut (G, arrowhead). The presence of lung bud formation is
further confirmed by WMISH of Nkx2.1 in RA-supplemented
Raldh2-/- foregut (G, inset, arrowhead). Dotted lines
outline the lung. (H) Real-time PCR showing downregulation of
Tgfbi in RA-treated lung mesenchymal (MLg) cells (*,
P<0.05 by Student's t-test). Ht, heart; St, stomach; Ctr,
control. Scale bar: 300 µm in E.
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