ArticleJournal of the American College of Cardiology2011
Disruption of platelet-derived growth factor-dependent phosphatidylinositol 3-kinase and phospholipase Cγ 1 activity abolishes vascular smooth muscle cell proliferation and migration and attenuates neointima formation in vivo.
Article in Journal of the American College of Cardiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 46 citations in OpenAlex.
- Temperature as a Key Modulator: Investigating Phosphorylation Patterns of p.Asn666Human mutation · 2025Article
- The Future of Microsurgery: Vascularized Composite Allotransplantation and Engineering Vascularized Tissue.Journal of hand and microsurgery · 2024Article
- KIF11 promotes vascular smooth muscle cell proliferation by regulating cell cycle progression and accelerates neointimal formation after arterial injury in mice.Frontiers in pharmacology · 2024Article
- Corneal Vascularization Associated With a Novel PDGFRB Variant.Investigative ophthalmology & visual science · 2023Article
- Yohimbine, an α2-Adrenoceptor Antagonist, Suppresses PDGF-BB-Stimulated Vascular Smooth Muscle Cell Proliferation by Downregulating the PLCγ1 Signaling Pathway.International journal of molecular sciences · 2022Article
- Long Non-Coding RNAs Might Regulate Phenotypic Switch of Vascular Smooth Muscle Cells Acting as ceRNA: Implications for In-Stent Restenosis.International journal of molecular sciences · 2022Article
- PDGF regulates guanylate cyclase expression and cGMP signaling in vascular smooth muscle.Communications biology · 2022Article
- Potential Effects of Metformin on the Vitality, Invasion, and Migration of Human Vascular Smooth Muscle Cells via Downregulating lncRNA-ATB.Disease markers · 2022Article
- FGF9 promotes cell proliferation and tumorigenesis in TM3 mouse Leydig progenitor cells.American journal of cancer research · 2022Article
- Disrupted PI3K subunit p110α signaling protects against pulmonary hypertension and reverses established disease in rodents.The Journal of clinical investigation · 2021Article
- Lipoprotein receptor signalling in atherosclerosis.Cardiovascular research · 2020Review
- The Enigmatic Role of Serum & Glucocorticoid Inducible Kinase 1 in the Endometrium.Frontiers in cell and developmental biology · 2020Review
- Activation of Bone Marrow-Derived Cells and Resident Aortic Cells During Aortic Injury.The Journal of surgical research · 2020Article
- Wild-type p53-induced phosphatase 1 promotes vascular smooth muscle cell proliferation and neointima hyperplasia after vascular injury via p-adenosine 5'-monophosphate-activated protein kinase/mammalian target of rapamycin complex 1 pathway.Journal of hypertension · 2019Article
- PI3Kγ (Phosphoinositide 3-Kinase γ) Regulates Vascular Smooth Muscle Cell Phenotypic Modulation and Neointimal Formation Through CREB (Cyclic AMP-Response Element Binding Protein)/YAP (Yes-Associated Protein) Signaling.Arteriosclerosis, thrombosis, and vascular biology · 2019Article
- Review
- FGF9/FGFR2 increase cell proliferation by activating ERK1/2, Rb/E2F1, and cell cycle pathways in mouse Leydig tumor cells.Cancer science · 2018Article
- PI3Kγ promotes vascular smooth muscle cell phenotypic modulation and transplant arteriosclerosis via a SOX9-dependent mechanism.EBioMedicine · 2018Article
- Tollip Negatively Regulates Vascular Smooth Muscle Cell-Mediated Neointima Formation by Suppressing Akt-Dependent Signaling.Journal of the American Heart Association · 2018Article
- Antiplatelet and anticoagulant for prevention of reocclusion in patients with atrial fibrillation undergoing endovascular treatment for low extremity ischemia.Journal of thoracic disease · 2018Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 3 countries.
Funding
Abstract
objectivesWe tested the hypothesis whether selective blunting of platelet-derived growth factor (PDGF)-dependent vascular smooth muscle cell (VSMC) proliferation and migration is sufficient to prevent neointima formation after vascular injury.
backgroundTo prevent neointima formation and stent thrombosis after coronary interventions, it is essential to inhibit VSMC proliferation and migration without harming endothelial cell function. The role of PDGF-a potent mitogen and chemoattractant for VSMC that does not affect endothelial cells-for neointima formation remains controversial.
methodsTo decipher the signaling pathways that control PDGF beta receptor (βPDGFR)-driven VSMC proliferation and migration, we characterized 2 panels of chimeric CSF1R/βPDGFR mutants in which the binding sites for βPDGFR-associated signaling molecules (Src, phosphatidylinositol 3-kinase [PI3K], GTPase activating protein of ras, SHP-2, phospholipase Cγ 1 [PLCγ]) were individually mutated. Based on in vitro results, the importance of PDGF-initiated signals for neointima formation was investigated in genetically modified mice.
resultsOur results indicate that the chemotactic response to PDGF requires the activation of Src, PI3K, and PLCγ, whereas PDGF-dependent cell cycle progression is exclusively mediated by PI3K and PLCγ. These 2 signaling molecules contribute to signal relay of the βPDGFR by differentially regulating cyclin D1 and p27(kip1). Blunting of βPDGFR-induced PI3K and PLCγ signaling by a combination mutant (F3) completely abolished the mitogenic and chemotactic response to PDGF. Disruption of PDGF-dependent PI3K and PLCγ signaling in mice expressing the F3 receptor led to a profound reduction of neointima formation after balloon injury.
conclusionsSignaling by the activated βPDGFR, particularly through PI3K and PLCγ, is crucial for neointima formation after vascular injury. Disruption of these specific signaling pathways is sufficient to attenuate pathogenic processes such as vascular remodeling in vivo.
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