ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2009
JunD and HIF-1alpha mediate transcriptional activation of angiotensinogen by TGF-beta1 in human lung fibroblasts.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 38 citations in OpenAlex.
- Flavonoids: Potential New Drug Candidates for Attenuating Vascular Remodeling in Pulmonary Hypertension.International journal of molecular sciences · 2025Review
- Dysregulated bidirectional epithelial-mesenchymal crosstalk: a core determinant of lung fibrosis progression.Chinese medical journal pulmonary and critical care medicine · 2024Article
- Topical captopril: a promising treatment for secondary lymphedema.Translational research : the journal of laboratory and clinical medicine · 2023Article
- Catalpol Attenuates Pulmonary Fibrosis by Inhibiting Ang II/ATFrontiers in medicine · 2022Article
- Spatial Transcriptome Uncovers the Mouse Lung Architectures and Functions.Frontiers in genetics · 2022Article
- Time-Dependent Pathological Changes in Hypoperfusion-Induced Abdominal Aortic Aneurysm.Biology · 2021Article
- The Role of Renin-Angiotensin-Aldosterone System in the Heart and Lung: Focus on COVID-19.Frontiers in pharmacology · 2021Review
- Cardiovascular implications of idiopathic pulmonary fibrosis: A way forward together?American heart journal · 2020Review
- Review
- Hypoxia and transforming growth factor β1 regulation of long non-coding RNA transcriptomes in human pulmonary fibroblasts.Physiological reports · 2020Article
- Neotuberostemonine inhibits the differentiation of lung fibroblasts into myofibroblasts in mice by regulating HIF-1α signaling.Acta pharmacologica Sinica · 2018Article
- Hypoxia-mediated translational activation of ITGB3 in breast cancer cells enhances TGF-β signaling and malignant featuresOncotarget · 2017Article
- The Processes and Mechanisms of Cardiac and Pulmonary Fibrosis.Frontiers in physiology · 2017Review
- Prior hypoxia prevents downregulation of ACE-2 by hyperoxia in fetal human lung fibroblasts.Experimental lung research · 2016Article
- Cross regulation between hypoxia-inducible transcription factor-1α (HIF-1α) and transforming growth factor (TGF)-ß1 mediates nickel oxide nanoparticles (NiONPs)-induced pulmonary fibrosis.American journal of translational research · 2015Article
- Modulation of angiotensin II signaling in the prevention of fibrosis.Fibrogenesis & tissue repair · 2015Article
- Quantitative profiling of chromatome dynamics reveals a novel role for HP1BP3 in hypoxia-induced oncogenesis.Molecular & cellular proteomics : MCP · 2014Article
- c-Jun N-Terminal Kinases Mediate a Wide Range of Targets in the Metastatic Cascade.Genes & cancer · 2013Review
- Article
- Fibrosis of two: Epithelial cell-fibroblast interactions in pulmonary fibrosis.Biochimica et biophysica acta · 2013Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Earlier work showed that TGF-beta1 potently increases angiotensinogen (AGT) gene mRNA in primary human lung fibroblasts. Here the mechanism of TGF-beta1-induced AGT expression was studied in the IMR90 human lung fibroblast cell line. The increase in AGT mRNA induced by TGF-beta1 was completely blocked by actinomycin-D. TGF-beta1 increased the activity of a full-length human AGT promoter-luciferase reporter (AGT-LUC) but did not alter AGT mRNA half-life. Serial deletion analyses revealed that 67% of TGF-beta-inducible AGT-LUC activity resides in a small domain of the AGT core promoter; this domain contains binding sites for hypoxia-inducible factor (HIF)-1 and activation protein-1 (AP-1) transcription factors. TGF-beta1 increased HIF-1alpha protein abundance and the activity of a hypoxia-responsive element reporter; overexpression of HIF-1 increased basal AGT-LUC activity. Both oligonucleotide pulldown and chromatin immunoprecipitation assays revealed increased binding of JunD and HIF-1alpha to the AGT core promoter in response to TGF-beta1. TGF-beta1-inducible AGT-LUC was reduced by an AP-1 dominant negative or by mutation of the AP-1 site. Knockdown of either JunD or HIF-1alpha individually by siRNA partially reduced AGT-LUC. In contrast, simultaneous knockdown of both JunD and HIF-1alpha completely eliminated TGF-beta1-inducible AGT-LUC activity. These data suggest that TGF-beta1 up-regulates AGT transcription in human lung fibroblasts through a mechanism that requires both JunD and HIF-1alpha binding to the AGT core promoter. They also suggest a molecular mechanism linking hypoxia signaling and fibrogenic stimuli in the lungs.
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