ArticleAmerican journal of translational research2016
Eotaxin-2 increased toll-like receptor 4 expression in endothelial cells
Article in American journal of translational research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- The role of canopy family proteins: biological mechanism and disease function.Molecular biology reports · 2025Review
- Multifaceted Nature of HuR in Atherosclerosis Development.Current medicinal chemistry · 2025Review
- TLR2 and TLR4 Are Expressed in Epiretinal Membranes: Possible Links with Vitreous Levels of Complement Fragments and DAMP-Related Proteins.International journal of molecular sciences · 2024Article
- The Role of CCL24 in Systemic Sclerosis.Rambam Maimonides medical journal · 2023Review
- OxLDL/β2GPI/anti‑β2GPI Ab complex induces inflammatory activation via the TLR4/NF‑κB pathway in HUVECs.Molecular medicine reports · 2021Article
- RNA-Seq Analyses Reveal That Endothelial Activation and Fibrosis Are Induced Early and Progressively byFrontiers in cellular and infection microbiology · 2020Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Eotaxin-2 is a potent chemoattractant. High concentration of eotaxin-2 triggers the inflammation and tumor metastasis. Inhibition of eotaxin-2 may protect experimental atherogenesis although the mechanism is still unclear. Toll-like receptor 4 (TLR4) plays a major role mediating vascular inflammation, which is related to atherogenesis. In the results, we demonstrated that eotaxin-2 potentially impairs the tube formation capacity of human coronary artery endothelial cells (HCAECs). Eotaxin-2 augments the monocytic adhesion in lipopolysaccharides (LPS)-induced HCAECs, and which were reversed by TLR4 siRNA. Thus this study was conducted to investigate whether eotaxin-2 increases TLR4 expression, and then enhances the sensitivity of cells to antigen stimulation in HCAECs, which mediates the increasing of the development of serious atherosclerosis. In fact, we showed that JNK/SAPK, p38 MAPK, and ERK1/2 activation contribute to the transcriptional signaling pathway, JNK/SAPK and p38 MAPK regulate post-transcriptional modification, as well as protein-trafficking pathway in eotaxin-2-treated HCAECs TLR4 expression. RNA binding proteins, such as human antigen R (HuR) and tristetraprolin (TTP) mediate stability of TLR4 mRNA and chaperone, such as PRAT4A (a protein associated with TLR4) regulate trafficking of TLR4 protein might confer eotaxin-2 responsiveness. Eotaxin-2 administration led to a significant elevation of high cholesterol diet-induced atherosclerosis, and of TLR4 expression in B6.129S7-
Indexed as
Identifiers
28078007PMC5209487W2582055998What OpenQuestion holds
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.