ArticleMolecular and cellular biochemistry2012
Urotensin upregulates transforming growth factor-β1 expression of asthma airway through ERK-dependent pathway.
Article in Molecular and cellular biochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Elevated Urotensin-II and TGF-β Levels in COPD: Biomarkers of Fibrosis and Airway Remodeling in Smokers.Medicina (Kaunas, Lithuania) · 2024Article
- Effect of curcumin nanoparticles on proliferation and migration of mouse airway smooth muscle cells and airway inflammatory infiltration.Frontiers in pharmacology · 2024Article
- Molecular analysis of duodenal eosinophilia.The Journal of allergy and clinical immunology · 2023Article
- Wnt/β-catenin signaling pathway regulates asthma airway remodeling by influencing the expression of c-Myc and cyclin D1 via the p38 MAPK-dependent pathway.Experimental and therapeutic medicine · 2019Article
- The G Protein-Coupled Receptor UT of the Neuropeptide Urotensin II Displays Structural and Functional Chemokine Features.Frontiers in endocrinology · 2017Review
- Apigenin inhibits TGF-β1-induced proliferation and migration of airway smooth muscle cells.International journal of clinical and experimental pathology · 2015Article
- Effects of Urotensin II Receptor Antagonist, GSK1440115, in Asthma.Frontiers in pharmacology · 2013Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Airway smooth muscle cells (ASMCs) play a key role in the process of asthma airway remodeling. Urotensin II (UII) and transforming growth factor (TGF)-β are potent mitogens for ASMCs proliferation. The study was aimed to determine whether UII-upregulated TGF-β-mediated ASMCs proliferation and extracellular signal-regulated kinase (ERK) was required for such an effect. OVA-sensitized rats were challenged to induce asthma. Lung morphology and airway dynamic parameters were monitored. ASMCs from control and asthma rats were purified for the measurement of UII and TGF-β1 expression. In vitro experiments were conducted to determine the direct effect of UII on TGF-β1 expression by ASMCs. Finally, U0126, an ERK inhibitor was used to examine the role of ERK pathway in UII mediated TGF-β1 upregulation. We found that both UII and TGF-β1 were upregulated in asthma lung tissues. In vitro study on ASMCs further revealed that UII may render its effect on ASMCs cells through the upregulation of TGF-β1. Data also supported the conclusion that ERK pathway was required, but not sufficient in UII-induced TGF-β1 upregulation. The current study provides new evidence that UII is involved in the TGF-β mediated mitogenic effect on ASMCs. UII, at least partially, uses ERK pathway to render such effect.
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