P6569Endothelial specific autotaxin in atherosclerosis

Karshovska, Ela; Mohibullah, R; Zahedi, Farima; Thomas, Dominique; Ferreiròs, Nerea; Schober, A.

doi:10.1093/eurheartj/ehy566.p6569

Cited by 1 publication

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“…The LPA classes consist of LPAs and cyclic-lysophosphatidic acids (cLPAs). They are formed by activated platelets and oxidation of low-density lipoproteins (LDLs) [38]. Once an inflammatory response is triggered, LPAs can activate platelets [39] and lead to endothelial dysfunction by activating NFκB [40][41][42][43].…”

Section: Impact Of Tnf On Lysophosphatidic Acids Sphingolipids and mentioning

confidence: 99%

Metabolic response of blood vessels to TNFα

Junaid

Schoeman

Yang

et al. 2020

eLife

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TNFa signaling in the vascular endothelium elicits multiple inflammatory responses that drive vascular destabilization and leakage. Bioactive lipids are main drivers of these processes. In vitro mechanistic studies of bioactive lipids have been largely based on two-dimensional endothelial cell cultures that, due to lack of laminar flow and the growth of the cells on non-compliant stiff substrates, often display a pro-inflammatory phenotype. This complicates the assessment of inflammatory processes. Three-dimensional microvessels-on-a-chip models provide a unique opportunity to generate endothelial microvessels in a more physiological environment. Using an optimized targeted liquid chromatography-tandem mass spectrometry measurements of a panel of pro- and anti-inflammatory bioactive lipids, we measure the profile changes upon administration of TNFa. We demonstrate that bioactive lipid profiles can be readily detected from three-dimensional microvessels-on-a-chip and display a more dynamic, less inflammatory response to TNFa, that resembles more the human situation, compared to classical two-dimensional endothelial cell cultures.

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