ArticleThe Journal of clinical investigation1995
Decreased type II/type I TGF-beta receptor ratio in cells derived from human atherosclerotic lesions. Conversion from an antiproliferative to profibrotic response to TGF-beta1.
Article in The Journal of clinical investigation, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 170 citations in OpenAlex.
- TGFB1 genetic polymorphisms and coronary heart disease risk: a meta-analysis.BMC medical genetics · 2012Pooled it
- Evidence Accumulates: Patients with Ascending Aneurysms Are Strongly Protected from Atherosclerotic Disease.International journal of molecular sciences · 2023Review
- Review
- CCN2 Increases TGF-β Receptor Type II Expression in Vascular Smooth Muscle Cells: Essential Role of CCN2 in the TGF-β Pathway Regulation.International journal of molecular sciences · 2021Article
- Dynamic Crosstalk between Vascular Smooth Muscle Cells and the Aged Extracellular Matrix.International journal of molecular sciences · 2021Review
- The role of platelets in thrombus fibrosis and vessel wall remodeling after venous thrombosis.Journal of thrombosis and haemostasis : JTH · 2021Article
- A multiphase model of growth factor-regulated atherosclerotic cap formation.Journal of mathematical biology · 2020Article
- TGFβ, smooth muscle cells and coronary artery disease: a review.Cellular signalling · 2019Review
- 7-Dehydrocholesterol (7-DHC), But Not Cholesterol, Causes Suppression of Canonical TGF-β Signaling and Is Likely Involved in the Development of Atherosclerotic Cardiovascular Disease (ASCVD).Journal of cellular biochemistry · 2017Article
- Fibulin-4 deficiency increases TGF-β signalling in aortic smooth muscle cells due to elevated TGF-β2 levels.Scientific reports · 2015Article
- Ascending Aortic Proaneurysmal Genetic Mutations with Antiatherogenic Effects.The International journal of angiology : official publication of the International College of Angiology, Inc · 2015Article
- Ascending thoracic aortic aneurysms protect against myocardial infarctions.The International journal of angiology : official publication of the International College of Angiology, Inc · 2014Article
- TGF-β/Smad3 inhibit vascular smooth muscle cell apoptosis through an autocrine signaling mechanism involving VEGF-A.Cell death & disease · 2014Article
- Article
- Transforming growth factor-β and smooth muscle differentiation.World journal of biological chemistry · 2012Article
- Transforming growth factor-β and atherosclerosis: interwoven atherogenic and atheroprotective aspects.Cell and tissue research · 2012Review
- Cell Growth of BG-1 Ovarian Cancer Cells was Promoted by 4-Tert-octylphenol and 4-Nonylphenol via Downregulation of TGF-β Receptor 2 and Upregulation of c-myc.Toxicological research · 2011Article
- Protein kinase C delta mediates arterial injury responses through regulation of vascular smooth muscle cell apoptosis.Cardiovascular research · 2010Article
- Arterial gene transfer of the TGF-beta signalling protein Smad3 induces adaptive remodelling following angioplasty: a role for CTGF.Cardiovascular research · 2009Article
- Established neointimal hyperplasia in vein grafts expands via TGF-beta-mediated progressive fibrosis.American journal of physiology. Heart and circulatory physiology · 2009Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Atherosclerosis and postangioplasty restenosis may result from abnormal wound healing. The present studies report that normal human smooth muscle cells are growth inhibited by TGF-beta1, a potent wound healing agent, and show little induction of collagen synthesis to TGF-beta1, yet cells grown from human vascular lesions are growth stimulated by TGF-beta1 and markedly increase collagen synthesis. Both cell types increase plasminogen activator inhibitor-1 production, switch actin phenotypes in response to TGF-beta1, and produce similar levels of TGF-beta activity. Membrane cross-linking of 125I-TGF-beta1 indicates that normal human smooth muscle cells express type I, II, and III receptors. The type II receptor is strikingly decreased in lesion cells, with little change in the type I or III receptors. RT-PCR confirmed that the type II TGF-beta1 receptor mRNA is reduced in lesion cells. Transfection of the type II receptor into lesion cells restores the growth inhibitory response to TGF-beta1, implying that signaling remains responsive. Because TGF-beta1 is overexpressed in fibroproliferative vascular lesions, receptor-variant cells would be allowed to grow in a slow, but uncontrolled fashion, while overproducing extracellular matrix components. This TGF-beta1 receptor dysfunction may be relevant for atherosclerosis, restenosis and related fibroproliferative diseases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.