ArticleJournal of vascular surgery2009
Proliferative capacity of vein graft smooth muscle cells and fibroblasts in vitro correlates with graft stenosis.
Article in Journal of vascular surgery, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 33 citations in OpenAlex.
- MicroRNA-15a and microRNA-16 impair human circulating proangiogenic cell functions and are increased in the proangiogenic cells and serum of patients with critical limb ischemia.Circulation research · 2013Trial
- Comprehensive transcriptomics and proteomics analysis of neointima formation in human saphenous vein: implications for bypass graft disease.American journal of physiology. Heart and circulatory physiology · 2026Article
- Nanomedicine-based strategies for the treatment of vein graft disease.Nature reviews. Cardiology · 2025Review
- Ginger protects against vein graft remodeling by precisely modulating ferroptotic stress in vascular smooth muscle cell dedifferentiation.Journal of pharmaceutical analysis · 2025Article
- Epigenome-Wide Changes in the Cell Layers of the Vein Wall When Exposing the Venous Endothelium to Oscillatory Shear Stress.Epigenomes · 2023Article
- Arterial cyclic stretch regulates Lamtor1 and promotes neointimal hyperplasia via circSlc8a1/miR-20a-5p axis in vein grafts.Theranostics · 2022Article
- The Role of Immunomodulation in Vein Graft Remodeling and Failure.Journal of cardiovascular translational research · 2021Review
- Autophagic degradation of KAT2A/GCN5 promotes directional migration of vascular smooth muscle cells by reducing TUBA/α-tubulin acetylation.Autophagy · 2020Article
- Reconstruction of a lncRNA-Associated ceRNA Network in Endothelial Cells under Circumferential Stress.Cardiology research and practice · 2020Article
- Review
- Versican is differentially regulated in the adventitial and medial layers of human vein grafts.PloS one · 2018Article
- Inflammation in Vein Graft Disease.Frontiers in cardiovascular medicine · 2018Review
- Recombinant soluble apyrase APT102 inhibits thrombosis and intimal hyperplasia in vein grafts without adversely affecting hemostasis or re-endothelialization.Journal of thrombosis and haemostasis : JTH · 2017Article
- Vein graft failure: from pathophysiology to clinical outcomes.Nature reviews. Cardiology · 2016Review
- Scavenger receptor class A member 5 (SCARA5) and suprabasin (SBSN) are hub genes of coexpression network modules associated with peripheral vein graft patency.Journal of vascular surgery · 2016Article
- Macrophage Notch Ligand Delta-Like 4 Promotes Vein Graft Lesion Development: Implications for the Treatment of Vein Graft Failure.Arteriosclerosis, thrombosis, and vascular biology · 2015Article
- A single nucleotide polymorphism in the p27(Kip1) gene is associated with primary patency of lower extremity vein bypass grafts.Journal of vascular surgery · 2013Article
- Therapeutic strategies to combat neointimal hyperplasia in vascular grafts.Expert review of cardiovascular therapy · 2012Review
- Vascular smooth muscle cell motility: From migration to invasion.Experimental and clinical cardiology · 2010Article
- Syndecan-1: an inhibitor of arterial smooth muscle cell growth and intimal hyperplasia.Arteriosclerosis, thrombosis, and vascular biology · 2009Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveAbout a quarter of peripheral vein grafts fail due in part to intimal hyperplasia. The proliferative capacity and response to growth inhibitors of medial smooth muscle cells and adventitial fibroblasts in vitro were studied to test the hypothesis that intrinsic differences in cells of vein grafts are associated with graft failure.
methodsCells were grown from explants of the medial and adventitial layers of samples of vein grafts obtained at the time of implantation. Vein graft patency and function were monitored over the first 12 months using ankle pressures and Duplex ultrasound to determine vein graft status. Cells were obtained from veins from 11 patients whose grafts remained patent (non-stenotic) and from seven patients whose grafts developed stenosis. Smooth muscle cells (SMCs) derived from media and fibroblasts derived from adventitia were growth arrested in serum-free medium and then stimulated with 1 muM sphingosine-1-phosphate (S1P), 10 nM thrombin, 10 ng/ml epidermal growth factor (EGF), 10 ng/ml platelet-derived growth factor-BB (PDGF-BB), PDGF-BB plus S1P, or PDGF-BB plus thrombin for determination of incorporation of [(3)H]-thymidine into DNA. Cells receiving PDGF-BB or thrombin were also treated with or without 100 microg/ml heparin, which is a growth inhibitor. Cells receiving thrombin were also treated with or without 150 nM AG1478, an EGF receptor kinase inhibitor.
resultsSMCs and fibroblasts from veins of patients that developed stenosis responded more to the growth factors, such as PDGF-BB alone or in combination with thrombin or S1P, than cells from veins of patients that remained patent (P = .012). In addition, while PDGF-BB-mediated proliferation of fibroblasts from grafts that remained patent was inhibited by heparin (P < .03), PDGF-BB-mediated proliferation of fibroblasts from veins that developed stenosis was not (P > .5).
conclusionInherent differences in the proliferative response of vein graft cells to PDGF-BB and heparin may explain, in part, the variability among patients regarding long term patency of vein grafts.
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