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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

机译:验证CD40体内 siRNA沉默和检测ApoE缺陷小鼠动脉粥样硬化进展的新标记的数据集

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摘要

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) . 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.
机译:此简短数据中提供的数据对应于CD40的``体内''沉默,可通过NFκB/ miR-125b轴减少实验性动脉粥样硬化的进展,并揭示动脉粥样硬化发病机理中的新潜在介体''(M.Hueso,L. De Ramon,E. Navarro,E. Ripoll,JM Cruzado,JM Grinyo,J. Torras,2016)。在这里,我们描述了在ApoE -/-小鼠主动脉及其对脾淋巴细胞亚群以及F4 / 80 + ,galectin-3 + 巨噬细胞或NF对主动脉内膜浸润的系统性作用-κB + 细胞,我们还显示了基因本体论和TLDA分析的输出,可检测动脉粥样硬化进展的潜在介质,我们为科学界提供了一组在其表达增加的基因动脉粥样硬化进展,但在CD40沉默后下调。

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