+1 Recommend
0 collections
      • Record: found
      • Abstract: found
      • Article: not found

      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

      Read this article at

          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.


          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.

          Related collections

          Author and article information



          Comment on this article