ArticleThe Journal of biological chemistry2016
Smooth Muscle Cell Proangiogenic Phenotype Induced by Cyclopentenyl Cytosine Promotes Endothelial Cell Proliferation and Migration.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
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- High fluid shear stress prevents atherosclerotic plaque formation by promoting endothelium denudation and synthetic phenotype of vascular smooth muscle cells.Molecular medicine reports · 2021Article
- Cellular Crosstalk between Endothelial and Smooth Muscle Cells in Vascular Wall Remodeling.International journal of molecular sciences · 2021Review
- Loss of Transforming Growth Factor Beta Signaling in Aortic Smooth Muscle Cells Causes Endothelial Dysfunction and Aortic Hypercontractility.Arteriosclerosis, thrombosis, and vascular biology · 2021Article
- The Effect of the Controlled Release of Platelet Lysate from PVA Nanomats on Keratinocytes, Endothelial Cells and Fibroblasts.Nanomaterials (Basel, Switzerland) · 2021Article
- Downregulation of lncRNA MIR181A2HG by high glucose impairs vascular endothelial cell proliferation and migration through the dysregulation of the miRNAs/AKT2 axis.International journal of molecular medicine · 2021Article
- Mueller polarimetric imaging for fast macroscopic mapping of microscopic collagen matrix remodeling by smooth muscle cells.Scientific reports · 2021Article
- PERK Inhibition Promotes Post-angioplasty Re-endothelialization via Modulating SMC Phenotype Changes.The Journal of surgical research · 2021Article
- LncRNA GAS5 attenuates fibroblast activation through inhibiting Smad3 signaling.American journal of physiology. Cell physiology · 2020Article
- LncRNA GAS5 regulates vascular smooth muscle cell cycle arrest and apoptosis via p53 pathway.Biochimica et biophysica acta. Molecular basis of disease · 2019Article
- The phenotype of vascular smooth muscle cells co-cultured with endothelial cells is modulated by PDGFR-β/IQGAP1 signaling in LPS-induced intravascular injury.International journal of medical sciences · 2019Article
- Recent advance in treatment of atherosclerosis: Key targets and plaque-positioned delivery strategies.Journal of tissue engineeringReview
- Pentoxifylline Prevents Restenosis by Inhibiting Cell Proliferation via p38MAPK Pathway in Rat Vein Graft Model.Cell transplantationArticle
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Vascular smooth muscle cells (SMCs) and endothelial cells (ECs) are in close contact with blood vessels. SMC phenotypes can be altered during pathological vascular remodeling. However, how SMC phenotypes affect EC properties remains largely unknown. In this study, we found that PDGF-BB-induced synthetic SMCs suppressed EC proliferation and migration while exhibiting increased expression of anti-angiogenic factors, such as endostatin, and decreased pro-angiogenic factors, including CXC motif ligand 1 (CXCL1). Cyclopentenyl cytosine (CPEC), a CTP synthase inhibitor that has been reported previously to inhibit SMC proliferation and injury-induced neointima formation, induced SMC redifferentiation. Interestingly, CPEC-conditioned SMC culture medium promoted EC proliferation and migration because of an increase in CXCL1 along with decreased endostatin production in SMCs. Addition of recombinant endostatin protein or blockade of CXCL1 with a neutralizing antibody suppressed the EC proliferation and migration induced by CPEC-conditioned SMC medium. Mechanistically, CPEC functions as a cytosine derivate to stimulate adenosine receptors A1 and A2a, which further activate downstream cAMP and Akt signaling, leading to the phosphorylation of cAMP response element binding protein and, consequently, SMC redifferentiation. These data provided proof of a novel concept that synthetic SMC exhibits an anti-angiogenic SMC phenotype, whereas contractile SMC shows a pro-angiogenic phenotype. CPEC appears to be a potent stimulator for switching the anti-angiogenic SMC phenotype to the pro-angiogenic phenotype, which may be essential for CPEC to accelerate re-endothelialization for vascular repair during injury-induced vascular wall remodeling.
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Registered trials
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