ArticleJournal of cellular physiology2008
Cholesterol modulates cellular TGF-beta responsiveness by altering TGF-beta binding to TGF-beta receptors.
Article in Journal of cellular physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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.
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Who cites it
39 citing papers in PubMed, 73 citations in OpenAlex.
- HDL Regulates TGFβ-Receptor Lipid Raft Partitioning, Restoring Contractile Features of Cholesterol-Loaded Vascular Smooth Muscle Cells.JACC. Basic to translational science · 2026Article
- TGF-beta inhibitors in cancer therapy: a review of the TGF-beta signal transduction pathway and current developments.EXCLI journal · 2026Review
- Oxymatrine impedes Alzheimer's progression via the attenuation of hypercholesterolemia and fibrosis.Metabolic brain disease · 2025Article
- NSDHL contributes to breast cancer stem-like cell maintenance and tumor-initiating capacity through TGF-β/Smad signaling pathway in MCF-7 tumor spheroid.BMC cancer · 2024Article
- Article
- Proactive and reactive roles of TGF-β in cancer.Seminars in cancer biology · 2023Review
- G9a Modulates Lipid Metabolism in CD4 T Cells to Regulate Intestinal Inflammation.Gastroenterology · 2023Article
- Myeloid masquerade: Microglial transcriptional signatures in retinal development and disease.Frontiers in cellular neuroscience · 2023Review
- TGF-β signaling in the tumor metabolic microenvironment and targeted therapies.Journal of hematology & oncology · 2022Review
- Cancer co-opts differentiation of B-cell precursors into macrophage-like cells.Nature communications · 2022Article
- CRISPR screens identify cholesterol biosynthesis as a therapeutic target on stemness and drug resistance of colon cancer.Oncogene · 2021Article
- Article
- Lipid mechanisms in hallmarks of cancer.Molecular omics · 2020Review
- Toward a Membrane-Centric Biology.Frontiers in immunology · 2020Article
- CtBP promotes metastasis of breast cancer through repressing cholesterol and activating TGF-β signaling.Oncogene · 2019Article
- Healthy Adult LDL-C Bears Reverse Association with Serum IL-17A Levels.Current chemical genomics and translational medicine · 2018Article
- Liver X receptors constrain tumor development and metastasis dissemination in PTEN-deficient prostate cancer.Nature communications · 2017Article
- The TGF-β Family inCold Spring Harbor perspectives in biology · 2017Review
- 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
- Pentabromophenol suppresses TGF-β signaling by accelerating degradation of type II TGF-β receptors via caveolae-mediated endocytosis.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Transforming growth factor-beta (TGF-beta) responsiveness in cultured cells can be modulated by TGF-beta partitioning between lipid raft/caveolae- and clathrin-mediated endocytosis pathways. The TbetaR-II/TbetaR-I binding ratio of TGF-beta on the cell surface has recently been found to be a signal that controls TGF-beta partitioning between these pathways. Since cholesterol is a structural component in lipid rafts/caveolae, we have studied the effects of cholesterol on TGF-beta binding to TGF-beta receptors and TGF-beta responsiveness in cultured cells and in animals. Here we demonstrate that treatment with cholesterol, alone or complexed in lipoproteins, decreases the TbetaR-II/TbetaR-I binding ratio of TGF-beta while treatment with cholesterol-lowering or cholesterol-depleting agents increases the TbetaR-II/TbetaR-I binding ratio of TGF-beta in all cell types studied. Among cholesterol derivatives and analogs examined, cholesterol is the most potent agent for decreasing the TbetaR-II/TbetaR-I binding ratio of TGF-beta. Cholesterol treatment increases accumulation of the TGF-beta receptors in lipid rafts/caveolae as determined by sucrose density gradient ultracentrifugation analysis of cell lysates. Cholesterol/LDL suppresses TGF-beta responsiveness and statins/beta-CD enhances it, as measured by the levels of P-Smad2 and PAI-1 expression in cells stimulated with TGF-beta. Furthermore, the cholesterol effects observed in cultured cells are also found in the aortic endothelium of atherosclerotic ApoE-null mice fed a high cholesterol diet. These results indicate that high plasma cholesterol levels may contribute to the pathogenesis of certain diseases (e.g., atherosclerosis) by suppressing TGF-beta responsiveness.
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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.