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. 2021 Nov 24;22(23):12685. doi: 10.3390/ijms222312685

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© 2021 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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Schematic illustration of IL-8 production in FLSs stimulated with PLA1A. Activated FLSs exposed PS on outer leaflet of cell membrane and presented this specific lipid substrate to extracellular PLA1A to produce lysoPS, which was subsequently converted by additional or FLSs-secreted ATX to produce LPA. LPA stimulated IL-8 production in an autocrine manner through activating LPA1/3 associated signaling pathway. IL-8 is a neutrophil chemotactic factor that plays a role in inflammation. Added heparin competitively bound to PLA1A to prevent surface-exposed PS from hydrolyzation. ATX inhibitor HA130 and LPA1/3 antagonist Ki16425 decreased secretion of IL-8 in FLSs through inhibiting ATX-LPAR axis.