biostudies-literatureHueso MShire Pharmaceutical SpainInstituto de Salud Carlos IIIEuropean Union (ERDF/ESF, “Investing in your future”)Societat Catalana de Transplantament1105-1112https://www.ebi.ac.uk/biostudies/studies/S-EPMC5128022biostudies-literatureUnknown9Data 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^-/- mouse aortas, and its systemic effects on splenic lymphocytic subpopulations as well as on the infiltration of aortic intima by F4/80⁺, galectin-3⁺ macrophages or by NF-κB⁺ cells. We also show the output of a Gene Ontology and TLDA analysis which allowed the detection of potential mediatorData in briefDatasets 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.PMC5128022PI11/00556PI14/00762PI13/00969Torras JCruzado JMRipoll EDe Ramon LNavarro EHueso MGrinyo JMfalseDatasets 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.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^-/- mouse aortas, and its systemic effects on splenic lymphocytic subpopulations as well as on the infiltration of aortic intima by F4/80⁺, galectin-3⁺ macrophages or by NF-κB⁺ cells. We also show the output of a Gene Ontology and TLDA analysis which allowed the detection of potential mediator2016-01-01T00:00:00Z2016 Dec2026-04-30T18:14:39.348Z2019-03-27T02:30:11ZS-EPMC51280222792429710.1016/j.dib.2016.11.045