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Trauelsen, Mette; Hiron, Thomas K; Lin, Da; Petersen, Jacob E; Breton, Billy; Husted, Anna Sofie; Hjorth, Siv A; Inoue, Asuka; Frimurer, Thomas M; Bouvier, Michel; O'Callaghan, Chris A; Schwartz, Thue W
Cell reports (Cambridge), 06/2021, Letnik: 35, Številka: 11Journal Article
Succinate functions both as a classical TCA cycle metabolite and an extracellular metabolic stress signal sensed by the mainly Gi-coupled succinate receptor SUCNR1. In the present study, we characterize and compare effects and signaling pathways activated by succinate and both classes of non-metabolite SUCNR1 agonists. By use of specific receptor and pathway inhibitors, rescue in G-protein-depleted cells and monitoring of receptor G protein activation by BRET, we identify Gq rather than Gi signaling to be responsible for SUCNR1-mediated effects on basic transcriptional regulation. Importantly, in primary human M2 macrophages, in which SUCNR1 is highly expressed, we demonstrate that physiological concentrations of extracellular succinate act through SUCNR1-activated Gq signaling to efficiently regulate transcription of immune function genes in a manner that hyperpolarizes their M2 versus M1 phenotype. Thus, sensing of stress-induced extracellular succinate by SUCNR1 is an important transcriptional regulator in human M2 macrophages through Gq signaling.
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