“…In conclusion, and in concordance with other investigators [20], our study indicates that the weakness of the ascending aortic tissue in TAA is linked with a perturbation of cell adhesion and cell interaction gene expression pathways. MicroRNAs probably act as regulators, possibly driving, or at least influencing, the development of the disease.…”
The development of thoracic aortic aneurysms (TAAs) involves a multifactorial process resulting in alterations of the structure and composition of the extracellular matrix (ECM). Recently, modifications in microRNA (miRNA) expression were implicated in the pathogenesis of TAA.This study presents a preliminary miRNA microarray analysis conducted on pooled ascending aorta RNAs obtained from non familial non syndromic TAA patients (five males and five females) compared to matched control pools. Ninety-nine differentially expressed miRNAs with >1.5-fold-up- or down-regulation in TAAs compared to controls were identified, 16.0% of which were similarly regulated in the two sexes.Genes putatively targeted by differentially expressed miRNAs belonged preferentially to focal adhesion and adherens junction pathways. The results indicate an altered regulation of miRNA-mediated gene expression in the cellular interactions of aneurysmal aortic wall.
“…In conclusion, and in concordance with other investigators [20], our study indicates that the weakness of the ascending aortic tissue in TAA is linked with a perturbation of cell adhesion and cell interaction gene expression pathways. MicroRNAs probably act as regulators, possibly driving, or at least influencing, the development of the disease.…”
The development of thoracic aortic aneurysms (TAAs) involves a multifactorial process resulting in alterations of the structure and composition of the extracellular matrix (ECM). Recently, modifications in microRNA (miRNA) expression were implicated in the pathogenesis of TAA.This study presents a preliminary miRNA microarray analysis conducted on pooled ascending aorta RNAs obtained from non familial non syndromic TAA patients (five males and five females) compared to matched control pools. Ninety-nine differentially expressed miRNAs with >1.5-fold-up- or down-regulation in TAAs compared to controls were identified, 16.0% of which were similarly regulated in the two sexes.Genes putatively targeted by differentially expressed miRNAs belonged preferentially to focal adhesion and adherens junction pathways. The results indicate an altered regulation of miRNA-mediated gene expression in the cellular interactions of aneurysmal aortic wall.
“…Additionally, the chord graph in Figure 6B shows the association of 18 genes with the top 8 GO terms. Interestingly, these results are similar to gene expression profiling of human TAA tissues where focal adhesion and adherens junction pathways were implicated (54,55). Accordingly, the observed differences in gene expression in the Notch1.129S6…”
“…Emr1 and Ptgs2 may represent targets to ameliorate the inflammatory response and limit the diameter expansion in Fbln4 Ϫ/Ϫ AA. It has been shown previously that diseased aortic tissue from TAA patients has different gene expression patterns than normal aortic tissue from control patients (1,9,43,58). Patients with connective tissue disorders, such as Marfan syndrome, or familial forms of TAA were excluded from these studies, so they do not provide insight into molecular mechanisms of aneurysm progression in these cases.…”
Kim J, Procknow JD, Yanagisawa H, Wagenseil JE. Differences in genetic signaling, and not mechanical properties of the wall, are linked to ascending aortic aneurysms in fibulin-4 knockout mice. Am
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