ArticleAmerican journal of physiology. Renal physiology2015
Angiotensin II increases fibronectin and collagen I through the β-catenin-dependent signaling in mouse collecting duct cells.
Article in American journal of physiology. Renal physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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37 citing papers in PubMed, 54 citations in OpenAlex.
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- Hypertension meets osteoarthritis - revisiting the vascular aetiology hypothesis.Nature reviews. Rheumatology · 2021Review
- High glucose induces trafficking of prorenin receptor and stimulates profibrotic factors in the collecting duct.Scientific reports · 2021Article
- Heme Oxygenase 1: A Defensive Mediator in Kidney Diseases.International journal of molecular sciences · 2021Review
- Angiotensin II type 1a receptor loss ameliorates chronic tubulointerstitial damage after renal ischemia reperfusion.Scientific reports · 2021Article
- A GSK3-SRF Axis Mediates Angiotensin II Induced Endothelin Transcription in Vascular Endothelial Cells.Frontiers in cell and developmental biology · 2021Article
- The Emerging Role of Innate Immunity in Chronic Kidney Diseases.International journal of molecular sciences · 2020Review
- Wnt/β-Catenin in Acute Kidney Injury and Progression to Chronic Kidney Disease.Seminars in nephrology · 2020Review
- Urinary angiotensinogen increases in the absence of overt renal injury in high fat diet-induced type 2 diabetic mice.Journal of diabetes and its complications · 2020Article
- Glycogen synthase kinase-3β: a promising candidate in the fight against fibrosis.Theranostics · 2020Review
- Involvement of hydrogen sulfide in the progression of renal fibrosis.Chinese medical journal · 2019Review
- Aliskiren Attenuates the Inflammatory Response and Wound Healing Process in Diabetic Mice With Periodontal Disease.Frontiers in pharmacology · 2019Article
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
The contribution of angiotensin II (ANG II) to renal and tubular fibrosis has been widely reported. Recent studies have shown that collecting duct cells can undergo mesenchymal transition suggesting that collecting duct cells are involved in interstitial fibrosis. The Wnt/β-catenin signaling pathway plays an essential role in development, organogenesis, and tissue homeostasis; however, the dysregulation of this pathway has been linked to fibrosis. In this study, we investigated whether AT1 receptor activation induces the expression of fibronectin and collagen I via the β-catenin pathway in mouse collecting duct cell line M-1. ANG II (10(-7) M) treatment in M-1 cells increased mRNA, protein levels of fibronectin and collagen I, the β-catenin target genes (cyclin D1 and c-myc), and the myofibroblast phenotype. These effects were prevented by candesartan, an AT1 receptor blocker. Inhibition of the β-catenin degradation with pyrvinium pamoate (pyr; 10(-9) M) prevented the ANG II-induced expression of fibronectin, collagen I, and β-catenin target genes. ANG II treatment promoted the accumulation of β-catenin protein in a time-dependent manner. Because phosphorylation of glycogen synthase kinase-3β (GSK-3β) inhibits β-catenin degradation, we further evaluated the effects of ANG II and ANG II plus pyr on p-ser9-GSK-3β levels. ANG II-dependent upregulation of β-catenin protein levels was correlated with GSK-3β phosphorylation. These effects were prevented by pyr. Our data indicate that in M-1 collecting duct cells, the β-catenin pathway mediates the stimulation of fibronectin and collagen I in response to AT1 receptor activation.
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