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Inflammatory markers in Down Syndrome: gene expression and functional analysis


The intrinsically deficient immune system in Down syndrome (DS) may contribute to the increased susceptibility to infections related to the main causes of hospitalization and death of these individuals and also seems to favor neurodegenerative processes like Alzheimer's Disease. Chromosome 21 trisomy can cause global changes in gene expression, including those not located on chromosome 21, which regulate immunology/inflammatory processes and other physiological processes. Thus, knowledge about the expression profile of inflammation-related genes and microRNAs that possibly regulate these genes may contribute to the understanding of an important mechanism of gene expression control in an aneuploidy condition and to provide information for the understanding of the molecular bases of clinical manifestations of the syndrome. The aim of this project is to investigate the expression of CCR7, IKBKB and PLA2G2D genes involved in the immune/inflammatory response, and microRNAs hsa-miR-378a-3p, hsa-miR-942-5p and hsa-miR-668-3p, in silico predicted to regulate these genes, respectively, in peripheral blood mononuclear cells of individuals with DS (case group) and individuals without the syndrome (control group) and to perform functional analysis in peripheral mononuclear blood cells of DS individuals to validate the regulation of the genes by these microRNAs. (AU)

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