ArticleJournal of cellular and molecular medicine2010
Imatinib inhibits vascular smooth muscle proteoglycan synthesis and reduces LDL binding in vitro and aortic lipid deposition in vivo.
Article in Journal of cellular and molecular medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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.
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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
26 citing papers in PubMed, 66 citations in OpenAlex.
- Article
- Mechanisms modulating foam cell formation in the arterial intima: exploring new therapeutic opportunities in atherosclerosis.Frontiers in cardiovascular medicine · 2024Review
- Non-Mouse Models of Atherosclerosis: Approaches to Exploring the Translational Potential of New Therapies.International journal of molecular sciences · 2022Review
- Endothelin-1 mediated glycosaminoglycan synthesizing gene expression involves NOX-dependent transactivation of the transforming growth factor-β receptor.Molecular and cellular biochemistry · 2022Article
- Determination of the Cut-off Value for Imatinib Plasma Levels Linked to Occurrence of Bone Pain in CML Patients.Drug design, development and therapy · 2022Article
- Endothelial Dysfunction and Cardiovascular Disease: History and Analysis of the Clinical Utility of the Relationship.Biomedicines · 2021Review
- Toll-like Receptor 4 Stimulates Gene Expression via Smad2 Linker Region Phosphorylation in Vascular Smooth Muscle Cells.ACS pharmacology & translational science · 2020Article
- The Role of Toll-like Receptors in Atherothrombotic Cardiovascular Disease.ACS pharmacology & translational science · 2020Review
- Mechanisms of Cardiovascular Toxicity of BCR-ABL1 Tyrosine Kinase Inhibitors in Chronic Myelogenous Leukemia.Current hematologic malignancy reports · 2020Review
- Factors Influencing the Steady-State Plasma Concentration of Imatinib Mesylate in Patients With Gastrointestinal Stromal Tumors and Chronic Myeloid Leukemia.Frontiers in pharmacology · 2020Article
- Mechanisms of PAR-1 mediated kinase receptor transactivation: Smad linker region phosphorylation.Journal of cell communication and signaling · 2019Article
- Transforming growth factor-β1 mediated CHST11 and CHSY1 mRNA expression is ROS dependent in vascular smooth muscle cells.Journal of cell communication and signaling · 2019Article
- BCR-ABL Tyrosine Kinase Inhibitors: Which Mechanism(s) May Explain the Risk of Thrombosis?TH open : companion journal to thrombosis and haemostasis · 2018Review
- The BCR-ABL1 Inhibitors Imatinib and Ponatinib Decrease Plasma Cholesterol and Atherosclerosis, and Nilotinib and Ponatinib Activate Coagulation in a Translational Mouse Model.Frontiers in cardiovascular medicine · 2018Article
- Intimal hyperplasia induced by vascular intervention causes lipoprotein retention and accelerated atherosclerosis.Physiological reports · 2017Article
- Roles of Cells from the Arterial Vessel Wall in Atherosclerosis.Mediators of inflammation · 2017Review
- Integrating the GPCR transactivation-dependent and biased signalling paradigms in the context of PAR1 signalling.British journal of pharmacology · 2016Review
- Multiple Growth Factors, But Not VEGF, Stimulate Glycosaminoglycan Hyperelongation in Retinal Choroidal Endothelial Cells.International journal of biological sciences · 2016Article
- Cellular and Molecular Pathology of Age-Related Macular Degeneration: Potential Role for Proteoglycans.Journal of ophthalmology · 2016Review
- Indispensable functions of ABL and PDGF receptor kinases in epithelial adherence of attaching/effacing pathogens under physiological conditions.American journal of physiology. Cell physiology · 2014Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
Abstract
The 'response to retention' hypothesis of atherogenesis proposes that proteoglycans bind and retain low-density lipoproteins (LDL) in the vessel wall. Platelet-derived growth factor (PDGF) is strongly implicated in atherosclerosis and stimulates proteoglycan synthesis. Here we investigated the action of the PDGF receptor inhibitor imatinib on PDGF-mediated proteoglycan biosynthesis in vitro, lipid deposition in the aortic wall in vivo and the carotid artery ex vivo. In human vSMCs, imatinib inhibited PDGF mediated (35)S-SO(4) incorporation into proteoglycans by 31% (P < 0.01) and inhibited PDGF-mediated size increases in both chemically cleaved and xyloside associated glycosaminoglycan (GAG) chains by 19%, P < 0.05 and 27%, P < 0.05, respectively. Imatinib decreased PDGF stimulation of the 6:4 position sulphation ratio of disaccharides. The half maximal saturation value for LDL binding for proteoglycans from PDGF stimulated cells in the presence of imatinib was approximately 2.5-fold higher than for PDGF treatment alone. In high fat fed ApoE(-/-) mice, imatinib reduced total lipid staining area by approximately 31% (P < 0.05). Carotid artery lipid accumulation in imatinib treated mice was also reduced. Furthermore, we demonstrate that imatinib inhibits phosphorylation of tyrosine 857, the autophosphorylation site of the PDGF receptor, in vSMCs. Thus imatinib inhibits GAG synthesis on vascular proteoglycans and reduces LDL binding in vitro and in vivo and this effect is mediated via the PDGF receptor. These findings validate a novel mechanism to prevent cardiac disease.
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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.