ArticleBiochimica et biophysica acta2013
Hypoxia-inducible factor prolyl-hydroxylase-2 mediates transforming growth factor beta 1-induced epithelial-mesenchymal transition in renal tubular cells.
Article in Biochimica et biophysica acta, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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45 citing papers in PubMed, 83 citations in OpenAlex.
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- Identification of potential mechanisms of Schisandrin B in the treatment of idiopathic pulmonary fibrosis by integrating network pharmacology and experimental validation.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Research progress of hypoxia-inducible factor-1α and zinc in the mechanism of diabetic kidney disease.Frontiers in pharmacology · 2025Review
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- The AKI-to-CKD Transition: The Role of Uremic Toxins.International journal of molecular sciences · 2023Review
- Molecular Characterization and Functional Analysis of Hypoxia-Responsive Factor Prolyl Hydroxylase Domain 2 in Mandarin Fish (Animals : an open access journal from MDPI · 2023Article
- Inhibition of LPS‑induced NLRP3 inflammasome activation by stem cell‑conditioned culture media in human gingival epithelial cells.Molecular medicine reports · 2023Article
- Loss of sphingosine kinase 2 protects against cisplatin-induced kidney injury.American journal of physiology. Renal physiology · 2022Article
- Oleuropein inhibits invasion of squamous cell carcinoma of the head and neck through TGF-β1 signaling pathway.BMC cancer · 2022Article
- Noncanonical TGF-β signaling leads to FBXO3-mediated degradation of ΔNp63α promoting breast cancer metastasis and poor clinical prognosis.PLoS biology · 2021Article
- Mechanisms of vasculogenic mimicry in hypoxic tumor microenvironments.Molecular cancer · 2021Review
- Methyl Jasmonate Cytotoxicity and Chemosensitization of T Cell LymphomaFrontiers in pharmacology · 2021Article
- Endothelial prolyl hydroxylase 2 is necessary for angiotensin II-mediated renal fibrosis and injury.American journal of physiology. Renal physiology · 2020Article
- Detrimental role of sphingosine kinase 1 in kidney damage in DOCA-salt hypertensive model: evidence from knockout mice.BMC nephrology · 2020Article
- Ginsenoside Rh1 Alleviates HK-2 Apoptosis by Inhibiting ROS and the JNK/p53 Pathways.Evidence-based complementary and alternative medicine : eCAM · 2020Article
- The Epithelial-to-Mesenchymal Transition as a Possible Therapeutic Target in Fibrotic Disorders.Frontiers in cell and developmental biology · 2020Review
- Stabilization of HIF-1α in Human Retinal Endothelial Cells Modulates Expression of miRNAs and Proangiogenic Growth Factors.Frontiers in pharmacology · 2020Article
- Extracts of Celastrus Orbiculatus Inhibit Cancer Metastasis by Down-regulating Epithelial-Mesenchymal Transition in Hypoxia-Induced Human Hepatocellular Carcinoma Cells.Chinese journal of integrative medicine · 2019Article
- NDNF inhibits the migration and invasion of human renal cancer cells through epithelial-mesenchymal transition.Oncology letters · 2019Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Transforming growth factor beta 1 (TGF-β1)-induced epithelial-mesenchymal transition (EMT) in kidney epithelial cells plays a key role in renal tubulointerstitial fibrosis in chronic kidney diseases. As hypoxia-inducible factor (HIF)-1α is found to mediate TGF-β1-induced signaling pathway, we tested the hypothesis that HIF-1α and its upstream regulator prolyl hydroxylase domain-containing proteins (PHDs) are involved in TGF-β1-induced EMT using cultured renal tubular cells. Our results showed that TGF-β1 stimulated EMT in renal tubular cells as indicated by the significant decrease in epithelial marker P-cadherin, and the increase in mesenchymal markers α-smooth muscle actin (α-SMA) and fibroblast-specific protein 1 (FSP-1). Meanwhile, we found that TGF-β1 time-dependently increased HIF-1α and that HIF-1α siRNA significantly inhibited TGF-β1-induced EMT, suggesting that HIF-1α mediated TGF-β1 induced-EMT. Real-time PCR showed that PHD1 and PHD2, rather than PHD3, could be detected, with PHD2 as the predominant form of PHDs (PHD1:PHD2=0.21:1.0). Importantly, PHD2 mRNA and protein, but not PHD1, were decreased by TGF-β1. Furthermore, over-expression of PHD2 transgene almost fully prevented TGF-β1-induced HIF-1α accumulation and EMT marker changes, indicating that PHD2 is involved in TGF-β1-induced EMT. Finally, Smad2/3 inhibitor SB431542 prevented TGF-β1-induced PHD2 decrease, suggesting that Smad2/3 may mediate TGF-β1-induced EMT through PHD2/HIF-1α pathway. It is concluded that TGF-β1 decreased PHD2 expression via an Smad-dependent signaling pathway, thereby leading to HIF-1α accumulation and then EMT in renal tubular cells. The present study suggests that PHD2/HIF-1α is a novel signaling pathway mediating the fibrogenic effect of TGF-β1, and may be a new therapeutic target in chronic kidney diseases.
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