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Figure 3


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.





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