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Endogenous itaconate is not required for particulate matter-induced NRF2 expression or inflammatory response

ABSTRACT: RNA-sequencing demonstrated Acod1 (Aconitate decarboxylase 1) as one of the top genes induced by air polution particulate matter (PM) in macrophages. We therefore sought to determine the effect of both exogenous itaconate (4-octyl itaconate) and endogenous itaconate on PM-induced inflammation in macrophages through RNA sequencing.

ORGANISM(S): Mus musculus

PROVIDER: GSE143881 | GEO | 2020/04/07

REPOSITORIES: GEO

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Itaconate suppresses atherosclerosis by impeding inflammation through Nrf2 signaling

Project description:Itaconate has emerged as a critical immunoregulatory metabolite. Here, we examined the therapeutic potential of itaconate in atherosclerosis. We found that both itaconate and the enzyme that synthesizes it, aconitate decarboxylase 1 (Acod1, also known as “immune-responsive gene 1”/IRG1) are upregulated during atherogenesis in mice. Here we analzyed the anatomy of atherosclerotic plaques from wildtype and Acod1-/- mice through single cell RNA-seq.

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Aconitate decarboxylase 1 participates in the control of pulmonary Brucella infection in mice

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10x single-cell RNAseq profiling of hiPSC derived WT and ISG15 KO macrophages stimulated with interferon-a and treated with itaconic acid, 4-octyl itaconate and ruxolitinib

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Expression data from hiPSC derived WT and ISG15 KO endothelial cells stimulated with interferon-a and treated with itaconic acid, dimethyl itaconate, 4-octyl itaconate and ruxolitinib

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