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Homocysteine activates T cells by enhancing endoplasmic reticulum-mitochondria coupling and increasing mitochondrial respiration
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Homocysteine activates T cells by enhancing endoplasmic reticulum-mitochondria coupling and increasing mitochondrial respiration
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Journal Article
Homocysteine activates T cells by enhancing endoplasmic reticulum-mitochondria coupling and increasing mitochondrial respiration
2016
Overview
Hyperhomocysteinemia （HHcy） accelerates atherosclero- sis by increasing proliferation and stimulating cytokine secretion in Tcells. However, whether homocysteine （Hcy）- mediated T cell activation is associated with metabolic reprogramming is unclear. Here, our in vivo and in vitro studies showed that Hcy-stimulated splenic T-cell activa- tion in mice was accompanied by increased levels of mitochondrial reactive oxygen species （ROS） and calcium, mitochondrial mass and respiration. Inhibiting mitochon- drial ROS production and calcium signals or blocking mitochondrial respiration largely blunted Hcy-induced T-cell interferon y （IFN-v） secretion and proliferation. Hcy also enhanced endoplasmic reticulum （ER） stress in T cells, and inhibition of ER stress with 4-phenylbutyric acid blocked Hcy-induced T-cell activation. Mechanistically, Hcy increased ER-mitochondria coupling, and uncou- pling ER-mitochondria by the microtubule inhibitor nocodazole attenuated Hcy-stimulated mitochondrial reprogramming, IFN-y secretion and proliferation in T cells, suggesting that juxtaposition of ER and mitochon-dria is required for Hcy-promoted mitochondrial function and T-cell activation. In conclusion, Hcy promotes T-cell activation by increasing ER-mitochondria coupling and regulating metabolic reprogramming.
Publisher
Higher Education Press,Springer Nature B.V,Oxford University Press
Subject
/ Biomedical and Life Sciences
/ Cell Proliferation - drug effects
/ Endoplasmic Reticulum - metabolism
/ endoplasmic reticulum stress
/ Endoplasmic Reticulum Stress - drug effects
/ Endoribonucleases - metabolism
/ Female
/ IFN-γ
/ Mice
/ Phenylbutyrates - pharmacology
/ Protein-Serine-Threonine Kinases - metabolism
/ Proto-Oncogene Proteins c-akt - metabolism
/ Reactive Oxygen Species - metabolism
/ T cell
/ T-Lymphocytes - drug effects
/ T细胞活化
/ 内质网应激
/ 动脉粥样硬化
/ 激活过程
/ 线粒体呼吸
/ 耦合
