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. Author manuscript; available in PMC: 2019 Nov 1.
Published in final edited form as: Dev Biol. 2018 Aug 25;443(1):50–63. doi: 10.1016/j.ydbio.2018.08.011

Figure 1. Deletion of Foxf1 from mesenchyme causes growth retardation and heart ventricular hypoplasia.

Figure 1.

A, Foxf1 is expressed in lung mesenchyme and endothelial cells during embryonic development. Paraffin lung sections from wild type mouse embryos (E11.5, E13.5 and E16.5) were stained with FOXF1 antibodies (dark brown) and counterstained with nuclear fast red (red). B-C, Schematic drawing illustrates deletion of Foxf1-floxed allele from mesenchymal cells. Foxf1fl/fl mice were bred with Dermo1-Cretg/- mice to generate Dermol-Cretg/- /Foxm1fl/fl double transgenic mice (Dermo1-Foxf1−/−). PCR shows deletion of Foxf1 and presence of Cre transgene. D, Foxf1 deletion from mesenchyme causes growth retardation. Representative photographs of E16.5 Dermo1-Foxf1−/− and Dermo1-Foxf1+/− embryos are shown. E-H, Hematoxylin and eosin (H&E) staining shows hypoplasia of the lung (E), liver (E), esophagus (F, top panels), lack of blood islands in liver tissue (F, bottom panels), interventricular septum defect (G) and myocardial hypoplasia (G-H) in E16.5 Dermo1-Foxf1−/− embryos. Thickness of the compact layer of ventricular myocardium (H) was quantitated using 10 random x400 microscope fields (n = 3 embryos in each group; * indicates p < 0.05). Abbreviations: Ep, epithelium; Me, mesenchyme; V, vein; Lu, lung; Li, liver; St, stomach; RV, right ventricle; LV, left ventricle; RA, right atrium; LA, left atrium; IVS, interventricular septum. Magnification: A (top panels) and G, x50; A (bottom panels), F and H, x400; E (top panels), x32; E (bottom panels), x16.