ArticleAmerican journal of physiology. Lung cellular and molecular physiology2007
TGF-beta1 stimulates human AT1 receptor expression in lung fibroblasts by cross talk between the Smad, p38 MAPK, JNK, and PI3K signaling pathways.
Article in American journal of physiology. Lung cellular and molecular physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 33 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
33 citing papers in PubMed, 83 citations in OpenAlex.
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- Attenuation of Allergen-, IL-13-, and TGF-α-induced Lung Fibrosis after the Treatment of rIL-15 in Mice.American journal of respiratory cell and molecular biology · 2019Article
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- HYDAMTIQ, a selective PARP-1 inhibitor, improves bleomycin-induced lung fibrosis by dampening the TGF-β/SMAD signalling pathway.Journal of cellular and molecular medicine · 2017Article
- Yishen Jiangzhuo Granules affect tubulointerstitial fibrosis via a mitochondrion-mediated apoptotic pathway.Chinese journal of integrative medicine · 2015Article
- Angiotensin II stimulates canonical TGF-β signaling pathway through angiotensin type 1 receptor to induce granulation tissue contraction.Journal of molecular medicine (Berlin, Germany) · 2015Article
- The kinase activity of the Ser/Thr kinase BUB1 promotes TGF-β signaling.Science signaling · 2015Article
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- Article
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- Hyperoxia and transforming growth factor β1 signaling in the post-ischemic mouse heart.Life sciences · 2013Article
- The possible potential therapeutic targets for drug induced gingival overgrowth.Mediators of inflammation · 2013Review
- Aldose reductase inhibition prevents allergic airway remodeling through PI3K/AKT/GSK3β pathway in mice.PloS one · 2013Article
- Transient receptor potential (TRP) channels and cardiac fibrosis.Current topics in medicinal chemistry · 2013Review
- Mast cells are required for the development of renal fibrosis in the rodent unilateral ureteral obstruction model.American journal of physiology. Renal physiology · 2012Article
- Article
Corrections and comments
- Retraction · 2012-04-01Falsification/Fabrication of Image · Investigation by Company/Institution · Investigation by ORI · Manipulation of Images · Misconduct - Official Investigation(s) and/or Finding(s) · Misconduct by Author · · ORI Finding of Misconduct: Terry S Elton
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- RetractedRetraction.2012
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Both angiotensin II (ANG II) and transforming growth factor-beta1 (TGF-beta1) are thought to be involved in mediating pulmonary fibrosis. Interactions between the renin-angiotensin system (RAS) and TGF-beta1 have been well documented, with most studies describing the effect of ANG II on TGF-beta1 expression. However, recent gene expression profiling experiments demonstrated that the angiotensin II type 1 receptor (AT(1)R) gene was a novel TGF-beta1 target in human adult lung fibroblasts. In this report, we show that TGF-beta1 augments human AT(1)R (hAT(1)R) steady-state mRNA and protein levels in a dose- and time-dependent manner in primary human fetal pulmonary fibroblasts (hPFBs). Nuclear run-on experiments demonstrate that TGF-beta1 transcriptionally activates the hAT(1)R gene and does not influence hAT(1)R mRNA stability. Pharmacological inhibitors and specific siRNA knockdown experiments demonstrate that the TGF-beta1 type 1 receptor (TbetaRI/ALK5), Smad2/3, and Smad4 are essential for TGF-beta1-stimulated hAT(1)R expression. Additional pharmacological inhibitor and small interference RNA experiments also demonstrated that p38 MAPK, JNK, and phosphatidylinositol 3-kinase (PI3K) signaling pathways are also involved in the TGF-beta1-stimulated increase in hAT(1)R density. Together, our results suggest an important role for cross talk among Smad, p38 MAPK, JNK, and PI3K pathways in mediating the augmented expression of hAT(1)R following TGF-beta1 treatment in hPFB. This study supports the hypothesis that a self-potentiating loop exists between the RAS and the TGF-beta1 signaling pathways and suggests that ANG II and TGF-beta1 may cooperate in the pathogenesis of pulmonary fibrosis. The synergy between these systems may require that both pathways be simultaneously inhibited to treat fibrotic lung disease.
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Registered trials
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