ArticlePloS one2014
Functional characterization of S100A8 and S100A9 in altering monolayer permeability of human umbilical endothelial cells.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 84 citations in OpenAlex.
- Potential for anti‑angiogenic therapy targeting the receptor for advanced glycation end products/VEGF axis in ulcerative colitis (Review).Molecular medicine reports · 2026Review
- Acid ceramidase overactivity drives ceramide loss, leading to atopic dry skin and Th2-skewed immune polarization.The Journal of pathology · 2026Article
- Single-cell RNA sequencing reveals multiple pathways involving pulmonary immune and epithelial cells through which aryl hydrocarbon receptor activation attenuates acute respiratory distress syndrome.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- A Novel Rat Model for Human Meibomian Gland Dysfunction and Ocular Rosacea.Investigative ophthalmology & visual science · 2026Article
- Hepatic vein-derived factors may affect pulmonary arteriovenous malformations after single ventricle palliation by modulating vascular cell behavior.Scientific reports · 2025Article
- Article
- Neutrophil-Endothelium Interaction Mediated by S100A9 Promotes Pulmonary Vascular Remodeling During Pulmonary Hypertension.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Review
- S100 calcium-binding protein A8 exacerbates deep vein thrombosis in vascular endothelial cells.Scientific reports · 2025Article
- Advances in the study of S100A9 in cardiovascular diseases.Cell proliferation · 2024Review
- Preliminary clinical analysis and pathway study of S100A8 as a biomarker for the diagnosis of acute deep vein thrombosis.Scientific reports · 2024Article
- Computational Deciphering of the Role of S100A8 and S100A9 Proteins and Their Changes in the Structure Assembly Influences Their Interaction with TLR4, RAGE, and CD36.The protein journal · 2024Article
- High S100A9 level predicts poor survival, and the S100A9 inhibitor paquinimod is a candidate for treating idiopathic pulmonary fibrosis.BMJ open respiratory research · 2024Article
- Beyond the barrier: the immune-inspired pathways of tumor extravasation.Cell communication and signaling : CCS · 2024Review
- Deficiency of S100A8/A9 attenuates pulmonary microvascular leakage in septic mice.Respiratory research · 2023Article
- S100 proteins in cardiovascular diseases.Molecular medicine (Cambridge, Mass.) · 2023Review
- Chronic E-Cigarette Use Impairs Endothelial Function on the Physiological and Cellular Levels.Arteriosclerosis, thrombosis, and vascular biology · 2022Article
- Exploratory Investigation of the Plasma Proteome Associated with the Endotheliopathy of Trauma.International journal of molecular sciences · 2022Article
- Tasquinimod efficacy and S100A9 expression in glucose-treated HREC cells.International ophthalmology · 2022Article
- The S100A10-AnxA2 complex is associated with the exocytosis of hepatitis B virus in intrauterine infection.Laboratory investigation; a journal of technical methods and pathology · 2022Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
S100A8, S100A9 and S100A8/A9 complexes have been known as important endogenous damage-associated molecular pattern (DAMP) proteins. But the pathophysiological roles of S100A8, S100A9 and S100A8/A9 in cardiovascular diseases are incompletely explained. In this present study, the effects of homo S100A8, S100A9 and their hetero-complex S100A8/A9 on endothelial barrier function were tested respectively in cultured human umbilical venous endothelial cells (HUVECs). The involvement of TLR4 and RAGE were observed by using inhibitor of TLR4 and blocking antibody of RAGE. The clarification of different MAPK subtypes in S100A8/A9-induced endothelial response was implemented by using specific inhibitors. The calcium-dependency was detected in the absence of Ca2+ or in the presence of gradient-dose Ca2+. The results showed that S100A8, S100A9 and S100A8/A9 could induce F-actin and ZO-1 disorganization in HUVECs and evoked the increases of HUVEC monolayer permeability in a dose- and time-dependent manner. The effects of S100A8, S100A9 and S100A8/A9 on endothelial barrier function depended on the activation of p38 and ERK1/2 signal pathways through receptors TLR4 and RAGE. Most importantly, we revealed the preference of S100A8 on TLR4 and S100A9 on RAGE in HUVECs. The results also showed the calcium dependency in S100A8- and S100A9-evoked endothelial response, indicating that calcium dependency on formation of S100A8 or A9 dimmers might be the prerequisite for this endothelial functional alteration.
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