ArticleMolecular biology of the cell2024
Increased basal fibronectin is sufficient to promote excess endothelial cell matrix assembly causing localized barrier dysfunction.
Article in Molecular biology of the cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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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.
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Who cites it
9 citing papers in PubMed.
- Integrin inhibition differentially remodels vascular networks in lung metastases driven by vessel co-option or angiogenesis.Angiogenesis · 2026Article
- Fast label-free live imaging with FlowVision reveals key principles of cancer cell arrest on endothelial monolayers.The EMBO journal · 2026Article
- Digital spatial profiling identifies features of primary and locoregional metastatic vasculature in triple negative breast cancer.Clinical & experimental metastasis · 2026Article
- Integrated bioinformatic analysis of biomarkers, pathways, and immune cell infiltration in ossification of the ligamentum flavum.International journal of clinical and experimental pathology · 2026Article
- Inhibition of S100A12 Attenuates LPS-induced Endothelial Barrier Dysfunction in HPMECs through the JAK2/STAT3 Signaling Pathway.Current molecular medicine · 2026Article
- Organoid-basedMicrobiology spectrum · 2025Article
- Bioinformatics analysis reveals major hub genes involved with extracellular matrix and inflammatory and endocrine pathways associated with intracranial aneurysm tissue.Interventional neuroradiology : journal of peritherapeutic neuroradiology, surgical procedures and related neurosciences · 2025Article
- Mechanism of disturbed endothelial cell function on angiogenesis following ischemic brain stroke (Review).Experimental and therapeutic medicine · 2025Review
- Sepsis-Induced Endothelial Barrier Dysfunction: Mechanisms, Pathology, and Therapeutic Advances.Research (Washington, D.C.) · 2025Review
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Endothelial cell behavior is regulated by subendothelial extracellular matrix (ECM). The ECM protein fibronectin (FN) is rare in healthy blood vessels but accumulates in disease accompanied by endothelial dysfunctions. Here, we report that excess assembly of FN disrupts key endothelial functions. We mimicked increased FN expression as in diseased stroma by providing exogenous FN basally in a Transwell insert and found dose-dependent upregulation of subendothelial FN matrix assembly. Taking advantage of discontinuous matrix assembly by endothelial cells, we show correlations between regional increases in FN matrix and disruptions in endothelial cell morphology, VE-cadherin junctions, and the cell cycle, all of which were not changed in FN-deficient regions of the monolayer. These changes affected endothelial barrier function with increased monolayer permeability exposing basal regions of high FN matrix and permitting FN-dependent adhesion of MDA-MB-231 tumor cells from the apical side of the monolayer. FN matrix accumulation was quick and increases in FN matrix preceded all other changes in the endothelium. Therefore, subendothelial accumulation of FN matrix is a cause, not an effect, of endothelial monolayer disorganization and leakiness. Regulating FN accumulation in the subendothelial space could be an important target for controlling progression of fibrosis and related diseases.
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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 Socratic graph.