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Inflammatory Wnt5A signalling pathways affecting barrier function of human vascular endothelial cells


Skaria, Tom; Schoedon, Gabriele (2017). Inflammatory Wnt5A signalling pathways affecting barrier function of human vascular endothelial cells. Journal of Inflammation:14:15.

Abstract

Wnt5A is a chemokine secreted by inflammatory-activated human macrophages that sustains their inflammatory response in an autocrine manner. High levels of Wnt5A are found in sera of patients with sepsis and septic shock. Here, we comment on recently reported Wnt5A signalling pathways in human vascular endothelial cells (VEC). In human VEC, Wnt5A regulates cytoskeleton remodelling and barrier function through Ryk receptor and Rho-associated protein serine/threonine kinase, targeting LIMK2 and CFL1 involved in actin polymerisation. Wnt5A/Ryk signalling in VEC can be antagonised by the naturally occurring Wnt inhibitory factor (WIF)-1 (WIF1). Therapeutic targeting of this mechanism may reduce vascular leakage and edema in severe systemic inflammation and therefore should be subject of further investigations. Keywords: Inflammation, Wnt5A, Endothelial barrier function, Ryk, IL-4, Wnt inhibitory factor-1.

Abstract

Wnt5A is a chemokine secreted by inflammatory-activated human macrophages that sustains their inflammatory response in an autocrine manner. High levels of Wnt5A are found in sera of patients with sepsis and septic shock. Here, we comment on recently reported Wnt5A signalling pathways in human vascular endothelial cells (VEC). In human VEC, Wnt5A regulates cytoskeleton remodelling and barrier function through Ryk receptor and Rho-associated protein serine/threonine kinase, targeting LIMK2 and CFL1 involved in actin polymerisation. Wnt5A/Ryk signalling in VEC can be antagonised by the naturally occurring Wnt inhibitory factor (WIF)-1 (WIF1). Therapeutic targeting of this mechanism may reduce vascular leakage and edema in severe systemic inflammation and therefore should be subject of further investigations. Keywords: Inflammation, Wnt5A, Endothelial barrier function, Ryk, IL-4, Wnt inhibitory factor-1.

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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > University Hospital Zurich > Clinic and Policlinic for Internal Medicine
Dewey Decimal Classification:610 Medicine & health
Language:English
Date:2017
Deposited On:13 Sep 2018 10:02
Last Modified:24 Sep 2019 23:36
Publisher:BioMed Central
ISSN:1476-9255
OA Status:Gold
Free access at:PubMed ID. An embargo period may apply.
Publisher DOI:https://doi.org/10.1186/s12950-017-0163-6
PubMed ID:28717346
Project Information:
  • : FunderSNSF
  • : Grant ID3100-043699
  • : Project TitlePublication of medical research funded by the Swiss National Science Foundation

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