Here, we show that expression of the transcription factor Basonuclin-1 (Bnc1) modulates TGF-β1-induced epithelial dedifferentiation of mammary epithelial cells.
Hepatocyte-specific basigin/CD147-knockout mice decreased the susceptibility to N-nitrosodiethylamine-induced tumorigenesis by suppressing TGF-β1-CD147 signaling and inhibiting dedifferentiation in hepatocytes during tumor progression.
Inhibition of TGF-β1 receptor kinase in HF MyoFb promotes dedifferentiation of MyoFb with loss of α-smooth muscle actin and depolymerization of stress fibers, and reduces the expression of profibrotic genes and cytokines levels to non-HF levels.
Further results suggested that miR-210 promoted the expression of TGF-β1 and its downstream effectors Snail1 and Slug which were highly elevated in the process of OS dedifferentiation.
Recently, it has been demonstrated this collaboration also takes place during fibrotic diseases, where TGF-β1 activates the WNT/β-catenin pathway that results in dedifferentiation of fibroblasts into myofibroblasts, increased production of extracellular matrix components and fibrosis.
In rats with renal mass reduction, protein accumulation in podocytes as a consequence of enhanced transcapillary passage preceded podocyte dedifferentiation and injury, increase in TGF-beta1 expression in podocytes, and TGF-beta1-dependent activation of mesangial cells.
Taken together, these results suggest that TGF-β1 may be involved in epithelial cell dedifferentiation, growth arrest and apoptosis in feline CKD as in human disease, and that cats may be a useful, naturally occurring model of human CKD.