ReviewInternational urology and nephrology2023
Tenascin-C promotes the proliferation and fibrosis of mesangial cells in diabetic nephropathy through the β-catenin pathway.
Review in International urology and nephrology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Sustained tenascin-C activation drives AKI-to-CKD progression via the Wnt/β-catenin pathway.International urology and nephrology · 2026Article
- Targeting inflammation-driven tumor progression with Zafirlukast via modulation of Jagged-1/Notch-1/Hes-1, Wnt-4/β-catenin, and VEGF signaling pathways in mice.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Renal Tissue-Derived Exosomal miRNA-34a in Diabetic Nephropathy Induces Renal Tubular Cell Fibrosis by Promoting the Polarization of M1 Macrophages.IET nanobiotechnology · 2024Article
- The Role of Tenascin-C in Hypertrophic Scar Formation: Insights from Cell and Animal Experiments.Clinical, cosmetic and investigational dermatology · 2024Article
Corrections and comments
- Erratum issued
Authors and funding
10 authors.
Funding
Abstract
objectiveTo mechanistically assess the involvement of tenascin-C (TNC) in diabetic nephropathy (DN).
methodsRenal specimens from DN patients were histopathologically examined, and their TNC expression patterns were evaluated via immunohistochemistry. Additionally, the hereditarily diabetic C57BL/KsJ db/db mice were induced to develop DN via adaptive feeding, and then their renal levels of TNC and β-catenin were assessed via western blotting and immunohistochemistry. Furthermore, the TNC and β-catenin levels in primary rat mesangial cells (RMCs) cultured with high glucose levels were assessed via western blotting. In parallel, RMCs cultured with TNC in the presence or absence of the β-catenin blocker ICG-001 were analyzed for their fibronectin and collagen I levels via immunostaining, and for their fibronectin, α-SMA, vimentin, PDGFR-β, PCNA, and β-catenin levels via western blotting.
resultsThe TNC levels in the specimens were associated with the pathological classification. In these DN specimens, TNC protein was highly detected in the MCs and slightly in the tubulointerstitium. Renal TNC (P < 0.05) and β-catenin (P < 0.001) were upregulated in db/db vs. db/m mice. High-glucose treatment upregulated TNC (P < 0.01) and β-catenin (P < 0.05) in RMCs. TNC treatment upregulated fibronectin (P < 0.05), α-SMA (P < 0.01), vimentin (P < 0.05), PCNA (P < 0.05), and β-catenin (P < 0.05) in RMCs, as assessed via western blotting. Immunohistochemical analysis confirmed the fibronectin upregulation and showed collagen I upregulation. Western-blot results also showed that levels of fibronectin (P < 0.001), α-SMA (P < 0.01), vimentin (P < 0.001), PCNA (P < 0.05), PDGFR-β (P < 0.05), and β-catenin (P < 0.01) were lower in RMCs co-treated with TNC and ICG-001 than in TNC-treated cells. Immunofluorescence analysis confirmed the decreased fibronectin level and showed that the collagen I level was also decreased by ICG-001.
conclusionTNC is upregulated in DN and induces MC proliferation and fibrosis through the β-catenin pathway.
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