Figure 1.
A diagram comparing eosinophil-deficient and wildtype intestinal structures, highlighting differences in smooth muscle cell development. The diagram shows two sections of the intestine, one labeled eosinophil-deficient and the other wildtype. In the eosinophil-deficient section, platelet-derived growth factor receptor alpha positive fibroblasts form the first wave of smooth muscle cells associated with the lacteal duct. In the wildtype section, eosinophils release transforming growth factor beta, promoting the outgrowth of platelet-derived growth factor receptor beta positive perivascular cells into a second wave of smooth muscle cells not associated with the lacteal duct. The wildtype section shows larger villus size due to the presence of this second wave of smooth muscle cells.

Eosinophil-derived TGFβ promotes a second wave of SMC differentiation. The first wave of SMC development is mostly completed by P9 and is independent of eosinophils. Here, PDGFRα+ subepithelial fibroblast–derived cells form the first SMC network associated with the lacteal duct. Eosinophil-deficient mice show reduced villus size due to the lack of the second wave of smooth muscle formation. Around P10, eosinophil-derived TGFβ promotes the outgrowth of PDGFRβ+ perivascular cells into SMCs via CNN1 star cells. This second wave of SMCs is not associated with the lacteal duct.

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