Datasets for the validation of the "in vivo" siRNA-silencing of CD40 and for the detection of new markers of atherosclerosis progression in ApoE-deficient mice
Miguel Hueso,
Laura De Ramon,
Estanislao Navarro,
Elia Ripoll,
Josep M. Cruzado,
Josep M. Grinyo,
Joan Torras
Affiliations
Miguel Hueso
Department of Nephrology, Hospital Universitari Bellvitge, and Bellvitge Research Institute (IDIBELL), L’Hospitalet de Llobregat, Spain
Laura De Ramon
Laboratory of Experimental Nephrology, Bellvitge Research Institute (IDIBELL), L’Hospitalet de Llobregat, Spain
Estanislao Navarro
Laboratory of Molecular Oncology, Bellvitge Research Institute (IDIBELL), L’Hospitalet de Llobregat, Spain
Elia Ripoll
Laboratory of Experimental Nephrology, Bellvitge Research Institute (IDIBELL), L’Hospitalet de Llobregat, Spain
Josep M. Cruzado
Department of Nephrology, Hospital Universitari Bellvitge, and Bellvitge Research Institute (IDIBELL), L’Hospitalet de Llobregat, Spain
Josep M. Grinyo
Department of Nephrology, Hospital Universitari Bellvitge, and Bellvitge Research Institute (IDIBELL), L’Hospitalet de Llobregat, Spain
Joan Torras
Department of Nephrology, Hospital Universitari Bellvitge, and Bellvitge Research Institute (IDIBELL), L’Hospitalet de Llobregat, Spain
Data presented in this Data in Brief article correspond to the article "in vivo" silencing of CD40 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 CD40 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 mediators of atherosclerosis progression. We provide the scientific community with a set of genes whose expression is increased during atherosclerosis progression but downregulated upon CD40 silencing.