ArticleJournal of inflammation (London, England)2017
WIF1 prevents Wnt5A mediated LIMK/CFL phosphorylation and adherens junction disruption in human vascular endothelial cells.
Article in Journal of inflammation (London, England), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Integrative multi-omics analysisiScience · 2025Article
- Overexpression of Wnt5a promoted the protective effect of mesenchymal stem cells on Lipopolysaccharide-induced endothelial cell injury via activating PI3K/AKT signaling pathway.BMC infectious diseases · 2024Article
- LIM kinases in cardiovascular health and disease.Frontiers in physiology · 2024Review
- The role of FOXO4/NFAT2 signaling pathway in dysfunction of human coronary endothelial cells and inflammatory infiltration of vasculitis in Kawasaki disease.Frontiers in immunology · 2022Article
- Wingless-related integration site (WNT) signaling is activated during the inflammatory response upon cardiac surgery: A translational study.Frontiers in cardiovascular medicine · 2022Article
- Gene Ontology Analysis for Drug Targets of the Whole Genome Transcriptome of Human Vascular Endothelial Cells in Response to Proinflammatory IL-1.Frontiers in pharmacology · 2019Article
- RSPO3 impairs barrier function of human vascular endothelial monolayers and synergizes with pro-inflammatory IL-1.Molecular medicine (Cambridge, Mass.) · 2018Article
- Inflammatory Wnt5A signalling pathways affecting barrier function of human vascular endothelial cells.Journal of inflammation (London, England) · 2017Article
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Authors and funding
3 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundWnt5A is released by activated macrophages and elevated levels have been detected in sepsis patients with severe systemic inflammation. However, the signalling and functional effects of Wnt5A in the vascular endothelial cells (VEC) remained unclear. Recently, we showed that Wnt5A affects barrier function in human VEC through Ryk interaction. Wnt5A/Ryk signalling activates LIMK to inactivate the actin depolymerisation factor CFL by phosphorylation, promotes actin polymerisation and disrupts endothelial adherens junctions.
findingsHere, we investigate the antagonistic effect of the Ryk specific secreted Wnt antagonist Wnt inhibitory factor (WIF)-1 on Wnt5A-mediated activation/inactivation of LIMK/CFL, and adherens junction disruption in human VEC. In human coronary artery endothelial cells (HCAEC), treatment with Wnt5A enhanced the phosphorylation of LIMK and CFL that was significantly prevented by WIF1. The presence of WIF1 suppressed Wnt5A-mediated disruption of β-catenin and VE-cadherin adherens junctions in HCAEC, thereby preventing barrier dysfunction caused by Wnt5A.
conclusionWe conclude that WIF1 or molecules with similar properties could be potent tools for the prevention of vascular leakage due to Wnt5A-mediated actin cytoskeleton remodeling in diseases associated with systemic inflammation.
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