ArticleBiomedical journal2016
Stimulation of transforming growth factor-beta-1 and contact with type I collagen cooperatively facilitate irreversible transdifferentiation in proximal tubular cells.
Article in Biomedical journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 9 citations in OpenAlex.
- Inhibition of lysyl oxidase‑like 2 ameliorates folic acid‑induced renal tubulointerstitial fibrosis.Experimental and therapeutic medicine · 2022Article
- Assessment of cadmium-induced nephrotoxicity using a kidney-on-a-chip device.Toxicology research · 2017Article
- Helicobacter pylori's road to colonization.Biomedical journal · 2016Article
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBy transdifferentiation, proximal tubular cells (PTC) have been considered as a source of interstitial myofibroblasts. We examined the combined effect of transforming growth factor-beta-1 (TGF-β1) stimulation and contact with type I collagen on PTC transdifferentiation.
methodsHuman kidney-2 cells were grown on type I substratum with the concurrent stimulation of TGF-β1.
resultsFollowing addition of TGF-β1, cells acquired an elongated fibroblastic appearance and an increase in α-smooth muscle actin (α-SMA) expression, a myofibroblastic marker. Upon addition of TGF-β1, E-cadherin expression, an epithelial marker, was reduced, while cytokeratin expression, another epithelial marker, remained unaltered. Following removal of TGF-β1, PTC regained an epithelial appearance and E-cadherin expression reverted to the unstimulated level, suggesting incomplete and reversible transdifferentiation. Addition of TGF-β1 to cells grown on type I collagen demonstrated a cooperatively increased α-SMA expression and decreased E-cadherin and cytokeratin expressions, suggesting more complete transdifferentiation. Co-stimulation of TGF-β1 and contact with type I collagen led to a stable cell phenotype and persistently decreased E-cadherin, which was not reversed upon removal of TGF-β1, indicating irreversible transdifferentiation. Addition of TGF-β1 or type I collagen caused a 4-fold increase in migratory cell number as compared to the control, whereas addition of both TGF-β1 and type I collagen led to an 11-fold increase.
conclusionsTGF-β1 alone results in a reversible and incomplete transdifferentiation. The combination of TGF-β1 and exposure to type I collagen leads to an irreversible and complete PTC transdifferentiation.
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