ArticleInternational journal of experimental pathology2006
TGFbeta1 induces epithelial-mesenchymal transition, but not myofibroblast transdifferentiation of human kidney tubular epithelial cells in primary culture.
Article in International journal of experimental pathology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed.
- Dual roles of renal tubular mitochondrial Akt1 in protecting against diabetic nephropathy and improving body glucose metabolism.The Journal of endocrinology · 2026Article
- Tacrolimus induces fibroblast-to-myofibroblast transition via a TGF-β-dependent mechanism to contribute to renal fibrosis.American journal of physiology. Renal physiology · 2023Article
- Cancer-Associated Fibroblast Heterogeneity, Activation and Function: Implications for Prostate Cancer.Biomolecules · 2022Review
- Role of extracellular matrix components and structure in new renal modelsFrontiers in physiology · 2022Review
- Review
- Article
- Thrombospondin-1: A Key Protein That Induces Fibrosis in Diabetic Complications.Journal of diabetes research · 2020Review
- Metabolomics Study of Metabolic Changes in Renal Cells in Response to High-Glucose Exposure Based on Liquid or Gas Chromatography Coupled With Mass Spectrometry.Frontiers in pharmacology · 2019Article
- Effects of aristolochic acid I and/or hypokalemia on tubular damage in C57BL/6 rat with aristolochic acid nephropathy.The Korean journal of internal medicine · 2018Article
- Functional Role of Non-Coding RNAs during Epithelial-To-Mesenchymal Transition.Non-coding RNA · 2018Review
- Epithelial contribution to the profibrotic stiff microenvironment and myofibroblast population in lung fibrosis.Molecular biology of the cell · 2017Article
- An immunofluorescence assay for extracellular matrix components highlights the role of epithelial cells in producing a stable, fibrillar extracellular matrix.Biology open · 2017Article
- Human Organ Culture: Updating the Approach to Bridge the Gap fromFrontiers in medicine · 2017Review
- Cancer cells remodel themselves and vasculature to overcome the endothelial barrier.Cancer letters · 2016Review
- Development of an In Vitro Assay to Evaluate Contractile Function of Mesenchymal Cells that Underwent Epithelial-Mesenchymal Transition.Journal of visualized experiments : JoVE · 2016Article
- Tacrolimus Modulates TGF-β Signaling to Induce Epithelial-Mesenchymal Transition in Human Renal Proximal Tubule Epithelial Cells.Journal of clinical medicine · 2016Article
- Epigenetic repression of Krüppel-like factor 4 through Dnmt1 contributes to EMT in renal fibrosis.International journal of molecular medicine · 2015Article
- Spontaneous calcification process in primary renal cells from a medullary sponge kidney patient harbouring a GDNF mutation.Journal of cellular and molecular medicine · 2015Article
- Macrophages During the Fibrotic Process: M2 as Friend and Foe.Frontiers in immunology · 2015Review
- Direct transcriptional reprogramming of adult cells to embryonic nephron progenitors.Journal of the American Society of Nephrology : JASN · 2013Article
Corrections and comments
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8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The origin and fate of renal interstitial myofibroblasts (MFs), the effector cells of renal fibrosis, are still debated. Experimental evidence suggests that renal MFs derive from tubular epithelial cells throughout the epithelial-mesenchymal transition (EMT) process. Primary human tubular epithelial cells (HUTECs) were cultured for 4 and 6 days on plastic or type I collagen-coated plates with 1, 5, 10 and 50 ng/ml of transforming growth factor beta1 (TGFbeta1). The EMT process was monitored by morphology and immunophenotyping for alphaSMA, cytokeratin 8-18, E-cadherin, vimentin and collagen III. Quantitative comparative RT/PCR and real-time PCR were used to evaluate the expression of collagen III and IV, fibronectin, tenascin, MMP-2, CTGF, E-cadherin and cadherin 11 genes, as well as those of the Smad signalling pathway. TGFbeta1 was found capable of reactivating the mesenchymal programme switched off during tubulogenesis, but it induced no de novo expression of alphaSMA gene or myofibroblast phenotype. We demonstrate that the EMT process is conditioned by the extracellular matrix and characterized by TGFbeta1-driven Smad3 downregulation. Our study results suggest that TGFbeta1 could function as a classic embryonal inducer, initiating a cascade of de-differentiating events that might be further controlled by other factors in the cellular environment.
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