Fig. 3. Ctgf and Col1a2 are Tgfß targets upregulated in RA-deficient mouse foreguts. Each panel depicts WMISH (left) and the corresponding black and white enhanced-contrast image of the explants (right). Boxes outline the region that includes the lung domain. (A-D) WMISH reveals no Ctgf signals in the WT control foregut (A), but expression is significantly upregulated in the mesoderm at the presumptive lung region of the BMS493-treated foregut (B, asterisks) and non-RA-supplemented Raldh2^-/- foregut (C, asterisks). Ctgf expression is markedly suppressed by RA supplementation in Raldh2^-/- foregut (D). (E-H) Col1a2 expression is detected by WMISH in the mesoderm of WT control lung bud (E) and is also dramatically increased in BMS493-treated foreguts (F, asterisks) and in non-RA-supplemented Raldh2^-/- foreguts (G, asterisks). Expression of Col1a2 is markedly downregulated by addition of exogenous RA in Raldh2^-/- foregut (H). Ht, heart; Lu, lung; St, stomach; Ctr, control. Scale bar: 300 µm in C.