ArticleMolecular and cellular biology2012
Angiotensin II induces epithelial-to-mesenchymal transition in renal epithelial cells through reactive oxygen species/Src/caveolin-mediated activation of an epidermal growth factor receptor-extracellular signal-regulated kinase signaling pathway.
Article in Molecular and cellular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 104 citations in OpenAlex.
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- CD148 agonistic antibody alleviates renal injury induced by chronic angiotensin II infusion in mice.BMC nephrology · 2025Article
- Reactive oxygen species in hypertension.Nature reviews. Cardiology · 2025Review
- Dexmedetomidine ameliorates high glucose-induced epithelial-mesenchymal transformation in HK-2 cells through the Cdk5/Drp1/ROS pathway.Acta biochimica et biophysica Sinica · 2024Article
- Cellular cross-talk drives mesenchymal transdifferentiation in diabetic kidney disease.Frontiers in medicine · 2024Review
- Anlotinib Alleviates Renal Fibrosis via Inhibition of the ERK and AKT Signaling Pathways.Oxidative medicine and cellular longevity · 2023Article
- Receptor-Mediated Redox Imbalance: An Emerging Clinical Avenue against Aggressive Cancers.Biomolecules · 2022Review
- EGFR-mediated activation of adipose tissue macrophages promotes obesity and insulin resistance.Nature communications · 2022Article
- Signaling pathways of chronic kidney diseases, implications for therapeutics.Signal transduction and targeted therapy · 2022Review
- RETRACTED: The p53-Driven Anticancer Effect ofLife (Basel, Switzerland) · 2022Article
- Receptor Tyrosine Kinase Signaling and Targeting in Glioblastoma Multiforme.International journal of molecular sciences · 2021Review
- YAP Activation in Renal Proximal Tubule Cells Drives Diabetic Renal Interstitial Fibrogenesis.Diabetes · 2020Article
- The Blockade of TACE-Dependent EGF Receptor Activation by Losartan-Erlotinib Combination Attenuates Renal Fibrosis Formation in 5/6-Nephrectomized Rats Under Vitamin D Deficiency.Frontiers in medicine · 2020Article
- Angiotensin receptor autoantibodies as exposures that modify disease progression: Cross sectional, longitudinal andJournal of translational autoimmunity · 2019Article
- Article
- The Role of the EGF Receptor in Sex Differences in Kidney Injury.Journal of the American Society of Nephrology : JASN · 2019Article
- Profibrotic effects of angiotensin II and transforming growth factor beta on feline kidney epithelial cells.Journal of feline medicine and surgery · 2019Article
- TNFα promotes mucosal wound repair through enhanced platelet activating factor receptor signaling in the epithelium.Mucosal immunology · 2019Article
- Parathyroid hormone-related protein induces fibronectin up-regulation in rat mesangial cells through reactive oxygen species/Src/EGFR signaling.Bioscience reports · 2019Article
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Authors and funding
3 authors at 1 institution in 2 countries.
Funding
Abstract
Chronic activation of the renin-angiotensin system plays a deleterious role in progressive kidney damage, and the renal proximal tubule is known to play an important role in tubulointerstitial fibrosis; however, the underlying molecular mechanism is unclear. Here we report that in the proximal tubule-like LLCPKcl4 cells expressing angiotensin II (Ang II) type 1 receptor, Ang II induced changes in cell morphology and expression of epithelial-to-mesenchymal transition (EMT) markers, which were inhibited by the miotogen-activated protein (MAP) kinase/extracellular signal-regulated kinase (ERK)-activating kinase (MEK) inhibitor PD98059 or the Src kinase inhibitor PP2. Ang II-stimulated phosphorylation of caveolin-1 (Cav) at Y14 and epidermal growth factor receptor (EGFR) at Y845 and induced association of these phosphoproteins in caveolin-enriched lipid rafts, thereby leading to prolonged EGFR-ERK signaling that was inhibited by Nox4 small interfering RNA (siRNA) and Src siRNA. Two different antioxidants not only inhibited phosphorylation of Src at Y416 but also blocked the EGFR-ERK signaling. Moreover, erlotinib (the EGFR tyrosine kinase inhibitor), EGFR siRNA, and Cav siRNA all inhibited both prolonged EGFR-ERK signaling and phenotypic changes induced by Ang II. Thus, this report provides the first evidence that reactive oxygen species (ROS)/Src-dependent activation of persistent Cav-EGFR-ERK signaling mediates renal tubular cell dedifferentiation and identifies a novel molecular mechanism that may be involved in progressive renal injury caused by chronic exposure to Ang II.
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