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Upregulated ethanolamine phospholipid synthesis by selenoprotein I is required for effective metabolic reprogramming during T cell activation.

Abstract：

OBJECTIVE:T cell activation triggers metabolic reprogramming to meet increased demands for energy and metabolites required for cellular proliferation. Ethanolamine phospholipid synthesis has emerged as a regulator of metabolic shifts in stem cells and cancer cells, which led us to investigate its potential role during T cell activation. METHODS:As selenoprotein I (SELENOI) is an enzyme participating in two metabolic pathways for the synthesis of phosphatidylethanolamine (PE) and plasmenyl PE, we generated SELENOI-deficient mouse models to determine loss-of-function effects on metabolic reprogramming during T cell activation. Ex vivo and in vivo assays were carried out along with metabolomic, transcriptomic, and protein analyses to determine the role of SELENOI and the ethanolamine phospholipids synthesized by this enzyme in cell signaling and metabolic pathways that promote T cell activation and proliferation. RESULTS:SELENOI knockout (KO) in mouse T cells led to reduced de novo synthesis of PE and plasmenyl PE during activation and impaired proliferation. SELENOI KO did not affect T cell receptor signaling, but reduced activation of the metabolic sensor AMPK. AMPK was inhibited by high [ATP], consistent with results showing SELENOI KO causing ATP accumulation, along with disrupted metabolic pathways and reduced glycosylphosphatidylinositol (GPI) anchor synthesis/attachment CONCLUSIONS: T cell activation upregulates SELENOI-dependent PE and plasmenyl PE synthesis as a key component of metabolic reprogramming and proliferation.

journal_name

Mol Metab

journal_title

Molecular metabolism

authors

Ma C,Hoffmann FW,Marciel MP,Page KE,Williams-Aduja MA,Akana ENL,Gojanovich GS,Gerschenson M,Urschitz J,Moisyadi S,Khadka VS,Rozovsky S,Deng Y,Horgen FD,Hoffmann PR

doi

10.1016/j.molmet.2021.101170

subject

Has Abstract

pub_date

2021-01-20 00:00:00

pages

101170

issn

2212-8778

pii

S2212-8778(21)00010-7

pub_type

杂志文章

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