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Oleic Acid Induces Tissue-Resident FOXP3 Regulatory T Cell Suppressive Functions (bulk RNA)

ABSTRACT: Comparing the transcriptomic program induced by oleic acid to that of the pro-inflammatory arachidonic acid, we find that Tregs sorted from peripheral blood and adipose of healthy donors transcriptomically resemble the oleic acid in vitro treated Tregs, whereas Tregs obtained from the adipose tissue of relapsing-remitting MS patients more closely resemble an arachidonic acid profile

ORGANISM(S): Homo sapiens

PROVIDER: GSE151586 | GEO | 2020/11/17

REPOSITORIES: GEO

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Oleic Acid Induces Tissue-Resident FOXP3 Regulatory T Cell Suppressive Functions

Project description:Comparing the transcriptomic program induced by oleic acid to that of the pro-inflammatory arachidonic acid, we find that Tregs sorted from peripheral blood and adipose of healthy donors transcriptomically resemble the oleic acid in vitro treated Tregs, whereas Tregs obtained from the adipose tissue of relapsing-remitting MS patients more closely resemble an arachidonic acid profile

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Oleic Acid Induces Tissue-Resident FOXP3 Regulatory T Cell Suppressive Functions (single-cell RNA)

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Project description:Iron overload, characterized by accumulation of iron in tissues, induces a multiorgan toxicity whose mechanisms are not fully understood. Using cultured cell lines, Caenorhabditis elegans, and mice, we found that ferroptosis occurs in the context of iron-overload-mediated damage. Exogenous oleic acid protected against iron-overload-toxicity in cell culture and Caenorhabditis elegans by suppressing ferroptosis. In mice, oleic acid protected against FAC-induced liver lipid peroxidation and damage. Oleic acid changed the cellular lipid composition, characterized by decreased levels of polyunsaturated fatty acyl phospholipids and decreased levels of ether-linked phospholipids. The protective effect of oleic acid in cells was attenuated by GW6471 (a PPAR- antagonist), as well as in Caenorhabditis elegans lacking the nuclear hormone receptor NHR-49 (a PPAR- functional homologue). These results highlight ferroptosis as a driver of iron-overload-mediated damage, which is inhibited by oleic acid. This monounsaturated fatty acid represents a potential therapeutic approach to mitigating organ damage in iron overload individuals.

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