ype A aortic dissection (TAAD) is a severe cardiovascular disease with high mortality rates. Current evidence suggests inflammation as the main mechanism of its complex pathophysiology. Accordingly, in this study the eventual presence of inflammatory cells in aorta specimens and any contribution of these cells in both apoptosis and metalloproteinase levels were assessed. The potential relationship between plasma inflammatory molecules and TAAD was also detected. In addition, implication in TAAD susceptibility of ten common and functional single nucleotide polymorphisms (SNP)s of six candidate genes (CCR5, TLR4, ACE, eNOs, MMP-9 and -2) was determined. Thus, histo-pathological and immunoistochemical aorta examination, TUNEL testing, genotyping of ten SNPs were performed. Levels of plasma inflammatory molecules were also determined using ELISA technique. A significant inflammatory infiltrate was observed in the examined aortas. Consistent with these data, significantly higher plasma levels of systemic inflammatory mediators characterized the cases. In addition, a high risk genotype significantly associated with TAAD susceptibility was identified. Thus, inflammation producing MMPs, cytokines and death mediators seem to be the shared pathological mechanism for TAAD in the population examined
Balistreri, C.R., Pisano, C., D’Amico, T., Palmeri, C., Candore, G., Maresi, E., et al. (2013). THE ROLE OF INFLAMMATION IN TYPE A AORTIC DISSECTION: A PILOT STUDY. EUROPEAN JOURNAL OF INFLAMMATION, 11(1), 269-277 [10.1177/1721727X1301100128].
THE ROLE OF INFLAMMATION IN TYPE A AORTIC DISSECTION: A PILOT STUDY
BALISTRERI, Carmela Rita;Pisano, C;PALMERI DI VILLALBA, Cesira;CANDORE, Giuseppina;MARESI, Emiliano;
2013-01-01
Abstract
ype A aortic dissection (TAAD) is a severe cardiovascular disease with high mortality rates. Current evidence suggests inflammation as the main mechanism of its complex pathophysiology. Accordingly, in this study the eventual presence of inflammatory cells in aorta specimens and any contribution of these cells in both apoptosis and metalloproteinase levels were assessed. The potential relationship between plasma inflammatory molecules and TAAD was also detected. In addition, implication in TAAD susceptibility of ten common and functional single nucleotide polymorphisms (SNP)s of six candidate genes (CCR5, TLR4, ACE, eNOs, MMP-9 and -2) was determined. Thus, histo-pathological and immunoistochemical aorta examination, TUNEL testing, genotyping of ten SNPs were performed. Levels of plasma inflammatory molecules were also determined using ELISA technique. A significant inflammatory infiltrate was observed in the examined aortas. Consistent with these data, significantly higher plasma levels of systemic inflammatory mediators characterized the cases. In addition, a high risk genotype significantly associated with TAAD susceptibility was identified. Thus, inflammation producing MMPs, cytokines and death mediators seem to be the shared pathological mechanism for TAAD in the population examinedFile | Dimensione | Formato | |
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