ArticleInternational journal of clinical and experimental pathology2015
P120 catenin attenuates lipopolysaccharide-induced blood-brain barrier dysfunction and inflammatory responses in human brain microvascular endothelial cells.
Article in International journal of clinical and experimental pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Functions of p120-catenin in physiology and diseases.Frontiers in molecular biosciences · 2024Review
- Nanoarchitecture and molecular interactions of epithelial cell junction proteins revealed by super-resolution microscopy.Annals of the New York Academy of Sciences · 2022Article
- Tissue Plasminogen Activator Causes Brain Microvascular Endothelial Cell Injury After Oxygen Glucose Deprivation by Inhibiting Sonic Hedgehog Signaling.Neurochemical research · 2019Article
- Acid fibroblast growth factor preserves blood-brain barrier integrity by activating the PI3K-Akt-Rac1 pathway and inhibiting RhoA following traumatic brain injury.American journal of translational research · 2017Article
- Environmental Correlation Analysis for Genes Associated with Protection against Malaria.Molecular biology and evolution · 2016Article
- P120 catenin attenuates the angiotensin II-induced apoptosis of human umbilical vein endothelial cells by suppressing the mitochondrial pathway.International journal of molecular medicine · 2016Article
- Activation of sonic hedgehog signaling attenuates oxidized low-density lipoprotein-stimulated brain microvascular endothelial cells dysfunction in vitro.International journal of clinical and experimental pathology · 2015Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increasing evidences suggest that p120 catenin (p120ctn) exerts important functions in the regulation of pro-inflammatory molecules. However, the relationship among p120ctn, inflammatory responses and blood-brain barrier (BBB) dysfunction as they are the initiator of sepsis is not unknown. In this study, we found that p120ctn expression was correlated with an increase in the permeability of BBB and a decrease in the expression of tight-junction proteins in human brain microvascular endothelial cells (HBMECs) after LPS challenge. Transfection with p120ctn small interfering RNA (siRNA) induced disruption of BBB integrity, monocyte migration across BBB and inflammatory responses at basal level and after LPS treatment. Conversely, over-expression of p120ctn with adenovirus significantly ameliorated BBB disruption and inflammatory responses in LPS-treated cells. Mechanistically, up-regulation of p120ctn inhibited LPS-induced NF-κB activation by suppressing IKKβ and IκBα phosphorylation, IκBα degradation. Therefore, we conclude that p120ctn improves the BBB dysfunction and inflammatory responses through the inhibition of NF-κB activation, suggesting that forced p120ctn expression may provide a novel therapeutic strategy to attenuate LPS-induced BBB compromise and sepsis.
Indexed as
Identifiers
26097613PMC4467000W2396154671What 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.