Figure 8
Schematic model depicts that tubular β-catenin controls interstitial fibroblast fate via epithelial-mesenchymal communication.
In control mice, tubular activation of β-catenin after injury leads to EMT (solid arrow) and upregulates tubular MMP-7 expression and secretion. This induces FasL expression in fibroblasts and potentiates their apoptosis. However, in Ksp-β-cat-/- mice, despite less EMT (empty arrow), fibroblasts have a prolonged life-span due to diminished apoptosis. Therefore, the pool size of interstitial fibroblasts in Ksp-β-cat-/- is unchanged, which results in similar fibrotic lesions. It is assumed that loss of tubular β-catenin does not affect fibroblast generation from other sources.
