Trial reportJournal of biomechanics2012
OxLDL and substrate stiffness promote neutrophil transmigration by enhanced endothelial cell contractility and ICAM-1.
Trial report in Journal of biomechanics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
26 citing papers in PubMed, 42 citations in OpenAlex.
- Substrate stiffness and cellular microenvironment regulate cell and junction mechanics in iPSC-derived brain microvascular endothelial cells.bioRxiv : the preprint server for biology · 2026Article
- Regulation of neutrophil function by the extracellular matrix.Biochemical Society transactions · 2025Review
- Age-dependent loss of HAPLN1 erodes vascular integrity via indirect upregulation of endothelial ICAM1 in melanoma.Nature aging · 2024Article
- Collagen concentration regulates neutrophil extravasation and migration in response to infection in an endothelium dependent manner.Frontiers in immunology · 2024Article
- Review
- The Innate Immune System in Cardiovascular Diseases and Its Role in Doxorubicin-Induced Cardiotoxicity.International journal of molecular sciences · 2022Review
- Pulmonary hypertension: Linking inflammation and pulmonary arterial stiffening.Frontiers in immunology · 2022Review
- Paradigms of endothelial stiffening in cardiovascular disease and vascular aging.Frontiers in physiology · 2022Review
- Morphological Phenotyping of Organotropic Brain- and Bone-Seeking Triple Negative Metastatic Breast Tumor Cells.Frontiers in cell and developmental biology · 2022Article
- Novel function of fluvastatin in attenuating oxidized low-density lipoprotein-induced endothelial cell ferroptosis in a glutathione peroxidase4- and cystine-glutamate antiporter-dependent manner.Experimental and therapeutic medicine · 2021Article
- Article
- Microphysiological Systems for Studying Cellular Crosstalk During the Neutrophil Response to Infection.Frontiers in immunology · 2021Review
- Involvement of Extracellular Vesicles in Vascular-Related Functions in Cancer Progression and Metastasis.International journal of molecular sciences · 2019Review
- Endothelial cell-secreted MIF reduces pericyte contractility and enhances neutrophil extravasation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Interleukin-37: The Effect of Anti-Inflammatory Response in Human Coronary Artery Endothelial Cells.Mediators of inflammation · 2019Review
- Altered DNA Methylation Sites in Peripheral Blood Leukocytes from Patients with Simple Steatosis and Nonalcoholic Steatohepatitis (NASH).Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Loss of giant obscurins alters breast epithelial cell mechanosensing of matrix stiffness.Oncotarget · 2017Article
- Mechanical heterogeneities in the subendothelial matrix develop with age and decrease with exercise.Journal of biomechanics · 2016Article
- Stiff substrates enhance monocytic cell capture through E-selectin but not P-selectin.Integrative biology : quantitative biosciences from nano to macro · 2016Article
- Nanoscale Imaging Reveals a Tetraspanin-CD9 Coordinated Elevation of Endothelial ICAM-1 Clusters.PloS one · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Elevated levels of oxLDL in the bloodstream and increased vasculature stiffness are both associated with cardiovascular disease in patients. However, it is not known how oxLDL and subendothelial matrix stiffness together regulate an immune response. Here, we used an in vitro model of the vascular endothelium to explore the combined effects of oxLDL and subendothelial matrix stiffening on neutrophil transmigration. We prepared fibronectin-coated polyacrylamide gels of varying stiffness and plated human umbilical vein endothelial cells (ECs) onto the gels. We observed that oxLDL treatment of the endothelium promoted neutrophil transmigration (from <1% to 26% on soft 0.87kPa substrates), with stiffer substrates further promoting transmigration (54% on 5kPa and 41% on 280kPa). OxLDL exposure enhanced intercellular adhesion molecule-1 (ICAM-1) expression on the endothelium, which was likely responsible for the oxLDL-induced transmigration. Importantly, inhibition of MLCK-mediated EC contraction reduced transmigration to ∼9% on all substrates and eliminated the effects of subendothelial matrix stiffness. In addition, large holes, thousands of square microns in size, formed in monolayers on stiff substrates following transmigration, indicating that oxLDL treatment and subsequent neutrophil transmigration caused serious damage to the endothelium. Our results reveal that an interplay between ICAM-1 and MLCK-dependent contractile forces mediates neutrophil transmigration through oxLDL-treated endothelium. Thus, microvasculature stiffness, which likely varies depending on tissue location and health, is an important regulator of the transmigration step of the immune response in the presence of oxLDL.
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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.