{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Tarnawski L"],"funding":["The Swedish Research Council","Stiftelsen Lars Hiertas Minne","Richard and Helen DeVos Foundation","Knut och Alice Wallenbergs Stiftelse","Hjärt-Lungfonden","ALF project funds","G&amp;amp;#x00F6;sta Fraenckel Foundation","MedTechLabs","Foundation for Geriatric Diseases","Novo Nordisk Fonden","Loo och Hans Ostermans Stiftelse för Medicinsk Forskning"],"pagination":["e2212476120"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10083572"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["120(14)"],"pubmed_abstract":["Endothelial dysfunction and impaired vasodilation are linked with adverse cardiovascular events. T lymphocytes expressing choline acetyltransferase (ChAT), the enzyme catalyzing biosynthesis of the vasorelaxant acetylcholine (ACh), regulate vasodilation and are integral to the cholinergic antiinflammatory pathway in an inflammatory reflex in mice. Here, we found that human T cell ChAT mRNA expression was induced by T cell activation involving the PI3K signaling cascade. Mechanistically, we identified that ChAT mRNA expression was induced following the attenuation of RE-1 Silencing Transcription factor REST-mediated methylation of the ChAT promoter, and that ChAT mRNA expression levels were up-regulated by GATA3 in human T cells. In functional experiments, T cell-derived ACh increased endot"],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["Cholinergic regulation of vascular endothelial function by human ChAT<sup>+</sup> T cells."],"pmcid":["PMC10083572"],"funding_grant_id":["2014-JOVINGE","2019","FO2018-0494","20170199 20180502","2014","2019-01337 2021-00730","2017-03366 2020-04443 2020-01645","20200827 20190672","2019-01096 2021-00729","2019-01408 2021-00728","NNF18OC0055026","20210431"],"pubmed_authors":["Carlstrom M","Shavva VS","Nilsson I","Ahmed O","Malin SG","Weiland M","Jovinge S","Heller Sahlgren B","Schmidt S","Kehr J","Eberhardson M","Farnert A","Weitzberg E","Olofsson PS","Abbas K","Hult H","Wang FH","Gustafsson M","Caravaca AS","Chen P","Kort EJ","Tarnawski L","Zhuge Z","Gallina AL","Martinez-Enguita D"],"additional_accession":[]},"is_claimable":false,"name":"Cholinergic regulation of vascular endothelial function by human ChAT<sup>+</sup> T cells.","description":"Endothelial dysfunction and impaired vasodilation are linked with adverse cardiovascular events. T lymphocytes expressing choline acetyltransferase (ChAT), the enzyme catalyzing biosynthesis of the vasorelaxant acetylcholine (ACh), regulate vasodilation and are integral to the cholinergic antiinflammatory pathway in an inflammatory reflex in mice. Here, we found that human T cell ChAT mRNA expression was induced by T cell activation involving the PI3K signaling cascade. Mechanistically, we identified that ChAT mRNA expression was induced following the attenuation of RE-1 Silencing Transcription factor REST-mediated methylation of the ChAT promoter, and that ChAT mRNA expression levels were up-regulated by GATA3 in human T cells. In functional experiments, T cell-derived ACh increased endot","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Apr","modification":"2026-07-14T19:13:15.632Z","creation":"2025-04-04T14:29:52.512Z"},"accession":"S-EPMC10083572","cross_references":{"pubmed":["36989306"],"doi":["10.1073/pnas.2212476120"]}}