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      BMP-7 counteracts TGF-beta1-induced epithelial-to-mesenchymal transition and reverses chronic renal injury.

      Nature medicine

      Transforming Growth Factor beta1, Activin Receptors, Type I, pharmacology, metabolism, Transforming Growth Factor beta, Transfection, genetics, Trans-Activators, Smad5 Protein, Smad3 Protein, Signal Transduction, Recombinant Proteins, Receptors, Transforming Growth Factor beta, Protein-Serine-Threonine Kinases, Phosphoproteins, pathology, drug therapy, Nephritis, Mice, Inbred Strains, Mice, drug effects, cytology, Mesoderm, embryology, Kidney Tubules, physiology, Epithelial Cells, DNA-Binding Proteins, Chronic Disease, Cells, Cultured, Cell Differentiation, Cadherins, Bone Morphogenetic Proteins, Bone Morphogenetic Protein 7, Animals

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          Abstract

          Bone morphogenic protein (BMP)-7 is a 35-kDa homodimeric protein and a member of the transforming growth factor (TGF)-beta superfamily. BMP-7 expression is highest in the kidney, and its genetic deletion in mice leads to severe impairment of eye, skeletal and kidney development. Here we report that BMP-7 reverses TGF-beta1-induced epithelial-to-mesenchymal transition (EMT) by reinduction of E-cadherin, a key epithelial cell adhesion molecule. Additionally, we provide molecular evidence for Smad-dependent reversal of TGF-beta1-induced EMT by BMP-7 in renal tubular epithelial cells and mammary ductal epithelial cells. In the kidney, EMT-induced accumulation of myofibroblasts and subsequent tubular atrophy are considered key determinants of renal fibrosis during chronic renal injury. We therefore tested the potential of BMP-7 to reverse TGF-beta1-induced de novo EMT in a mouse model of chronic renal injury. Our results show that systemic administration of recombinant human BMP-7 leads to repair of severely damaged renal tubular epithelial cells, in association with reversal of chronic renal injury. Collectively, these results provide evidence of cross talk between BMP-7 and TGF-beta1 in the regulation of EMT in health and disease.

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          Author and article information

          Journal
          10.1038/nm888
          12808448

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