In this study, we investigated the correlations between the FBN1 genotype-phenotype and aortic events (aortic dissection and aortic aneurysm) in patients with Marfan syndrome.
To achieve this, we use a combination of balloon angioplasty, elastase and collagenase, and a lysyl oxidase inhibitor, called β-aminopropionitrile (BAPN), to create clinically significant infrarenal aortic aneurysms, analogous to human disease.
The results of the comparison with control group demonstrated that the increase in the expression levels of hsa‑miR‑143‑3p (P=0.017) and hsa‑miR‑22 (P=0.03) candidate miRNAs were statistically significant in the TAA group, but not in the TAD group.
The results of the comparison with control group demonstrated that the increase in the expression levels of hsa‑miR‑143‑3p (P=0.017) and hsa‑miR‑22 (P=0.03) candidate miRNAs were statistically significant in the TAA group, but not in the TAD group.
The high-throughput sequencing revealed 20 and 17 TAA-specific miRNAs in tissue and plasma samples, respectively. qRT-PCR analysis in extended cohort revealed sex-related differences in miR-10a-5p, miR-126-3p, miR-155-5p and miR-148a-3p expression, which were the most significantly dysregulated in TAA tissues of male patients.
BM-MSCs and MSCs-CM significantly attenuated matrix metalloproteinase (MMP)-2 and MMP-9 expression, aortic elastin degradation and AA growth at the site of AA.
The current study aimed to investigate the therapeutic effects and potential mechanisms of murine bone marrow MSC (BM-MSCs)-derived conditioned medium (MSCs-CM) on angiotensin II (AngII)-induced AA in apolipoprotein E-deficient (apoE<sup>-/-</sup> ) mice.
These treatments with BM-MSCs and MSCs-CM also decreased Ly6c<sup>high</sup> monocytes in peripheral blood on day 7 and M1 macrophage infiltration in AA tissues on day 14, whereas they increased M2 macrophages.
These treatments with BM-MSCs and MSCs-CM also decreased Ly6c<sup>high</sup> monocytes in peripheral blood on day 7 and M1 macrophage infiltration in AA tissues on day 14, whereas they increased M2 macrophages.
A significant increase in the renal function markers (BUN, 240%; creatinine, 187%; and creatine kinase, 117%), oxidative stress parameters (lipid peroxidation, 192% increase; catalase, 30.5% decrease), cytokines (IL-4, 120%; TNF-<i>α</i>, 129%; and IFN-<i>γ</i>, 133%), and DNA damage was observed in the TAA-treated group.
A significant increase in the renal function markers (BUN, 240%; creatinine, 187%; and creatine kinase, 117%), oxidative stress parameters (lipid peroxidation, 192% increase; catalase, 30.5% decrease), cytokines (IL-4, 120%; TNF-<i>α</i>, 129%; and IFN-<i>γ</i>, 133%), and DNA damage was observed in the TAA-treated group.
A significant increase in the renal function markers (BUN, 240%; creatinine, 187%; and creatine kinase, 117%), oxidative stress parameters (lipid peroxidation, 192% increase; catalase, 30.5% decrease), cytokines (IL-4, 120%; TNF-<i>α</i>, 129%; and IFN-<i>γ</i>, 133%), and DNA damage was observed in the TAA-treated group.
A significant increase in the renal function markers (BUN, 240%; creatinine, 187%; and creatine kinase, 117%), oxidative stress parameters (lipid peroxidation, 192% increase; catalase, 30.5% decrease), cytokines (IL-4, 120%; TNF-<i>α</i>, 129%; and IFN-<i>γ</i>, 133%), and DNA damage was observed in the TAA-treated group.