ArticleCirculation research2010
Atheroprone hemodynamics regulate fibronectin deposition to create positive feedback that sustains endothelial inflammation.
Article in Circulation research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
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Who cites it
77 citing papers in PubMed, 134 citations in OpenAlex.
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- Integrin-Specific Signaling Drives ER Stress-Dependent Atherogenic Endothelial Activation.bioRxiv : the preprint server for biology · 2025Article
- Fibronectin-dependent integrin signaling drives EphA2 expression in vascular smooth muscle cells.American journal of physiology. Cell physiology · 2025Article
- The impact of a high fat diet and platelet activation on pre-metastatic niche formation.Nature communications · 2025Article
- Phosphorylation of endothelial histone H3.3 serine 31 by PKN1 links flow-induced signaling to proatherogenic gene expression.Nature cardiovascular research · 2025Article
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- miR-328-5p functions as a critical negative regulator in early endothelial inflammation and advanced atherosclerosis.BMB reports · 2024Article
- Preliminary Exploration of Potential Active Ingredients and Molecular Mechanisms of Yanggan Yishui Granules for Treating Hypertensive Nephropathy Using UPLC-Q-TOF/MS Coupled with Network Pharmacology and Molecular Docking Strategy.Journal of analytical methods in chemistry · 2024Article
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- The Role of the Piezo1 Mechanosensitive Channel in Heart Failure.Current issues in molecular biology · 2023Review
- Extracellular matrix composition alters endothelial force transmission.American journal of physiology. Cell physiology · 2023Article
- Novel Aspects Targeting Platelets in Atherosclerotic Cardiovascular Disease-A Translational Perspective.International journal of molecular sciences · 2023Review
- Different roles of endothelial cell-derived fibronectin and plasma fibronectin in endothelial dysfunction.Turkish journal of medical sciences · 2023Article
17 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
rationaleThe extracellular matrix protein fibronectin (FN) is focally deposited in regions of atherosclerosis, where it contributes to inflammatory signaling.
objectiveTo elucidate the mechanism by which FN deposition is regulated by local shear stress patterns, its dependence on platelet-endothelial cell adhesion molecule (PECAM)-1 mechanotransduction and the role this pathway plays in sustaining an atheroprone/proinflammatory phenotype. METHODS AND
resultsHuman endothelial cells were exposed in vitro to atheroprone or atheroprotective shear stress patterns derived from human carotid arteries. Onset of atheroprotective flow induced a transient increase in FN deposition, whereas atheroprone flow caused a steady increase in FN expression and integrin activation over time, leading to a significant and sustained increase in FN deposition relative to atheroprotective conditions. Comparing FN staining in ApoE(-/-) and ApoE(-/-)PECAM(-/-) mice showed that PECAM-1 was essential for FN accumulation in atheroprone regions of the aortic arch. In vitro, small interfering RNA against PECAM-1 blocked the induction of FN and the activation of nuclear factor (NF)-kappaB by atheroprone flow, which was rescued by the addition of exogenous FN. Additionally, blocking NF-kappaB activation attenuated the flow-induced FN expression. Small interfering RNA against FN significantly reduced NF-kappaB activity, which was rescued by the addition of exogenous FN.
conclusionsThese results indicate that FN gene expression and assembly into matrix fibrils is induced by atheroprone fluid shear stress. This effect is mediated at least in part by the transcription factor NF-kappaB. Additionally, because FN promotes activation of NF-kappaB, atheroprone shear stress creates a positive feedback to maintain inflammation.
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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.