{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Hueso M"],"funding":["Shire Pharmaceutical Spain","Instituto de Salud Carlos III","European Union (ERDF/ESF, “Investing in your future”)","Societat Catalana de Transplantament"],"pagination":["1105-1112"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5128022"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["9"],"pubmed_abstract":["Data presented in this Data in Brief article correspond to the article \"in vivo\" silencing of <i>CD40</i> reduces progression of experimental atherogenesis through a NFκB/miR-125b axis and reveals new potential mediators in the pathogenesis of atherosclerosis\" (M. Hueso, L. De Ramon, E. Navarro, E. Ripoll, J.M. Cruzado, J.M. Grinyo, J. Torras, 2016) [1]. Here, we describe the validation of the silencing of <i>CD40</i> expression with a specific siRNA in ApoE<sup>-/-</sup> mouse aortas, and its systemic effects on splenic lymphocytic subpopulations as well as on the infiltration of aortic intima by F4/80<sup>+</sup>, galectin-3<sup>+</sup> macrophages or by NF-κB<sup>+</sup> cells. We also show the output of a Gene Ontology and TLDA analysis which allowed the detection of potential mediator"],"journal":["Data in brief"],"pubmed_title":["Datasets for the validation of the \"in vivo\" siRNA-silencing of <i>CD40</i> and for the detection of new markers of atherosclerosis progression in ApoE-deficient mice."],"pmcid":["PMC5128022"],"funding_grant_id":["PI11/00556","PI14/00762","PI13/00969"],"pubmed_authors":["Torras J","Cruzado JM","Ripoll E","De Ramon L","Navarro E","Hueso M","Grinyo JM"],"additional_accession":[]},"is_claimable":false,"name":"Datasets for the validation of the \"in vivo\" siRNA-silencing of <i>CD40</i> and for the detection of new markers of atherosclerosis progression in ApoE-deficient mice.","description":"Data presented in this Data in Brief article correspond to the article \"in vivo\" silencing of <i>CD40</i> reduces progression of experimental atherogenesis through a NFκB/miR-125b axis and reveals new potential mediators in the pathogenesis of atherosclerosis\" (M. Hueso, L. De Ramon, E. Navarro, E. Ripoll, J.M. Cruzado, J.M. Grinyo, J. Torras, 2016) [1]. Here, we describe the validation of the silencing of <i>CD40</i> expression with a specific siRNA in ApoE<sup>-/-</sup> mouse aortas, and its systemic effects on splenic lymphocytic subpopulations as well as on the infiltration of aortic intima by F4/80<sup>+</sup>, galectin-3<sup>+</sup> macrophages or by NF-κB<sup>+</sup> cells. We also show the output of a Gene Ontology and TLDA analysis which allowed the detection of potential mediator","dates":{"release":"2016-01-01T00:00:00Z","publication":"2016 Dec","modification":"2026-04-30T18:14:39.348Z","creation":"2019-03-27T02:30:11Z"},"accession":"S-EPMC5128022","cross_references":{"pubmed":["27924297"],"doi":["10.1016/j.dib.2016.11.045"]}}