ArticleThe American journal of pathology2000
Potential biological role of transforming growth factor-beta1 in human congenital kidney malformations.
Article in The American journal of pathology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 50 citations in OpenAlex.
- Aberrant Differentiation of Human Pluripotent Stem Cell-Derived Kidney Precursor Cells inside Mouse Vascularized Bioreactors.Nephron · 2020Article
- Overactivity or blockade of transforming growth factor-β each generate a specific ureter malformation.The Journal of pathology · 2019Article
- Growing a new human kidney.Kidney international · 2019Review
- SMAD proteins directly suppressOncotarget · 2018Article
- Exogenous transforming growth factor-β1 enhances smooth muscle differentiation in embryonic mouse jejunal explants.Journal of tissue engineering and regenerative medicine · 2018Article
- PAX2 maintains the differentiation of mouse oviductal epithelium and inhibits the transition to a stem cell-like state.Oncotarget · 2017Article
- Transcriptome-wide based identification of miRs in congenital anomalies of the kidney and urinary tract (CAKUT) in children: the significant upregulation of tissue miR-144 expression.Journal of translational medicine · 2016Article
- Comparative immunohistochemical study of multicystic dysplastic kidneys with and without obstruction.Fetal and pediatric pathology · 2011Article
- Mechanisms of renal injury and progression of renal disease in congenital obstructive nephropathy.Pediatric nephrology (Berlin, Germany) · 2010Review
- TGF-beta1 gene polymorphisms and primary vesicoureteral reflux in childhood.Pediatric nephrology (Berlin, Germany) · 2008Article
- Genetic regulation of patterned tubular branching in Drosophila.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- Serum and urine interleukin-6 and transforming growth factor-beta1 in young infants with pyelonephritis.International urology and nephrology · 2007Article
- Galectin-3 associates with the primary cilium and modulates cyst growth in congenital polycystic kidney disease.The American journal of pathology · 2006Article
- ACE inhibition modulates transforming growth factor-beta receptors in the young rat.Pediatric nephrology (Berlin, Germany) · 2003Article
- Increased c-Met tyrosine kinase expression in segmental renal dysplasia.Pediatric nephrology (Berlin, Germany) · 2003Article
- Dissection of key events in tubular epithelial to myofibroblast transition and its implications in renal interstitial fibrosis.The American journal of pathology · 2001Article
- Deregulation of renal transforming growth factor-beta1 after experimental short-term ureteric obstruction in fetal sheep.The American journal of pathology · 2001Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Transformations between epithelial and mesenchymal cells are widespread during normal development and adult disease, and transforming growth factor-beta1 (TGF-beta1) has been implicated in some of these phenotypic switches. Dysplastic kidneys are a common cause of chronic kidney failure in young children and result from perturbed epithelial-mesenchymal interactions. In this study, we found that components of the TGF-beta1 axis were expressed in these malformations: TGF-beta1 mRNA and protein were up-regulated in dysplastic epithelia and surrounding mesenchymal cells, whereas TGF-beta receptors I and II were expressed in aberrant epithelia. We generated a dysplastic kidney epithelial-like cell line that expressed cytokeratin, ZO1, and MET, and found that exogenous TGF-beta1 inhibited proliferation and decreased expression of PAX2 and BCL2, molecules characterizing dysplastic tubules in vivo. Furthermore, addition of TGF-beta1 specifically induced morphological changes compatible with a shift to a mesenchymal phenotype, accompanied by loss of ZO1 at cell borders and up-regulation of the mesenchymal markers alpha-smooth muscle actin and fibronectin. The descriptive and functional data presented in this report potentially implicate TGF-beta1 in the pathobiology of dysplastic kidneys and our results provide preliminary evidence that an epithelial-to-mesenchymal phenotypic switch may be implicated in a clinically important developmental aberration.
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