ArticleCirculation2010
Smooth muscle cells orchestrate the endothelial cell response to flow and injury.
Article in Circulation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 62 citations in OpenAlex.
- Review
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- Vascular wall microenvironment: Endothelial cells original exosomes mediated melatonin-suppressed vascular calcification and vascular ageing in a m6A methylation dependent manner.Bioactive materials · 2024Article
- Has collateral blood flow any effect on restenosis rate? Our experience.Frontiers in neurology · 2024Article
- Endothelial mechanobiology in atherosclerosis.Cardiovascular research · 2023Review
- Monocyte-endothelial cell interactions in vascular and tissue remodeling.Frontiers in immunology · 2023Review
- The Biofabrication of Diseased Artery In Vitro Models.Micromachines · 2022Review
- Empagliflozin prevents neointima formation by impairing smooth muscle cell proliferation and accelerating endothelial regeneration.Frontiers in cardiovascular medicine · 2022Article
- 3D Bioprinted Multicellular Vascular Models.Advanced healthcare materials · 2021Article
- Cellular Crosstalk between Endothelial and Smooth Muscle Cells in Vascular Wall Remodeling.International journal of molecular sciences · 2021Review
- Network determinants of cardiovascular calcification and repositioned drug treatments.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Aerobic Exercise Training Inhibits Neointimal Formation via Reduction of PCSK9 and LOX-1 in Atherosclerosis.Biomedicines · 2020Article
- The Role and Regulation of Pulmonary Artery Smooth Muscle Cells in Pulmonary Hypertension.International journal of hypertension · 2020Review
- Sam68 impedes the recovery of arterial injury by augmenting inflammatory response.Journal of molecular and cellular cardiology · 2019Article
- Quantitative study of the capillaries within the white matter of the Tg2576 mouse model of Alzheimer's disease.Brain and behavior · 2019Article
- A paradigm of endothelium-protective and stent-free anti-restenotic therapy using biomimetic nanoclusters.Biomaterials · 2018Article
- Endovascular stent-induced alterations in host artery mechanical environments and their roles in stent restenosis and late thrombosis.Regenerative biomaterials · 2018Review
- A biomimetic microfluidic model to study signalling between endothelial and vascular smooth muscle cells under hemodynamic conditions.Lab on a chip · 2018Article
- The stentable in vitro artery: an instrumented platform for endovascular device development and optimization.Journal of the Royal Society, Interface · 2016Article
- Endothelial and Smooth Muscle Cell Interactions in the Pathobiology of Pulmonary Hypertension.American journal of respiratory cell and molecular biology · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundLocal modulation of vascular mammalian target of rapamycin (mTOR) signaling reduces smooth muscle cell (SMC) proliferation after endovascular interventions but may be associated with endothelial cell (EC) toxicity. The trilaminate vascular architecture juxtaposes ECs and SMCs to enable complex paracrine coregulation but shields SMCs from flow. We hypothesized that flow differentially affects mTOR signaling in ECs and SMCs and that SMCs regulate mTOR in ECs. METHODS AND
resultsSMCs and/or ECs were exposed to coronary artery flow in a perfusion bioreactor. We demonstrated by flow cytometry, immunofluorescence, and immunoblotting that EC expression of phospho-S6 ribosomal protein (p-S6RP), a downstream target of mTOR, was doubled by flow. Conversely, S6RP in SMCs was growth factor but not flow responsive, and SMCs eliminated the flow sensitivity of ECs. Temsirolimus, a sirolimus analog, eliminated the effect of growth factor on SMCs and of flow on ECs, reducing p-S6RP below basal levels and inhibiting endothelial recovery. EC p-S6RP expression in stented porcine arteries confirmed our in vitro findings: Phosphorylation was greatest in ECs farthest from intact SMCs in metal stented arteries and altogether absent after sirolimus stent elution.
conclusionsThe mTOR pathway is activated in ECs in response to luminal flow. SMCs inhibit this flow-induced stimulation of endothelial mTOR pathway. Thus, we now define a novel external stimulus regulating phosphorylation of S6RP and another level of EC-SMC crosstalk. These interactions may explain the impact of local antiproliferative delivery that targets SMC proliferation and suggest that future stents integrate design influences on flow and drug effects on their molecular targets.
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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.