Endothelial cell activation by interleukin-1 and extracellular matrix laminin-10 occurs via the YAP signalling pathway.

Autor: Thurgur H; Geoffrey Jefferson Brain Research Centre, The Manchester Academic Health Science Centre, Northern Care Alliance NHS Group, Manchester, United Kingdom; Division of Neuroscience, Faculty of Biology, Medicine and Health; A.V. Hill Building, University of Manchester, Oxford Road, Manchester M13 9PT, United Kingdom., Penny J; Division of Pharmacy and Optometry, Faculty of Biology, Medicine and Health, Stopford Building, University of Manchester, Oxford Road, Manchester M13 9PT, United Kingdom., Pinteaux E; Geoffrey Jefferson Brain Research Centre, The Manchester Academic Health Science Centre, Northern Care Alliance NHS Group, Manchester, United Kingdom; Division of Neuroscience, Faculty of Biology, Medicine and Health; A.V. Hill Building, University of Manchester, Oxford Road, Manchester M13 9PT, United Kingdom. Electronic address: emmanuel.pinteaux@manchester.ac.uk.
Jazyk: angličtina
Zdroj: Journal of neuroimmunology [J Neuroimmunol] 2022 Dec 15; Vol. 373, pp. 577993. Date of Electronic Publication: 2022 Oct 28.
DOI: 10.1016/j.jneuroim.2022.577993
Abstrakt: Laminin-10 (LM-10) is a key regulator of blood-brain barrier (BBB) repair after hypoxia and inflammation. Here we investigated the signalling mechanisms regulated by LM-10 in human brain endothelial cell line hCMEC/D3 in response to interleukin(IL)-1beta(β) in vitro. LM-10 promoted endothelial proliferation and repair of an endothelial monolayer after scratch injury, and upregulated IL-1β-induced ICAM-1 and VCAM-1 expression. IL-1β and LM-10 regulated YAP signalling pathway in endothelial cells leading to differential expression of YAP target genes, ctgf and serpine-1, providing evidence that the YAP signalling pathway could be a new therapeutic target for the treatment of BBB dysfunction in CNS diseases.
(Crown Copyright © 2022. Published by Elsevier B.V. All rights reserved.)
Databáze: MEDLINE
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