6533b855fe1ef96bd12afff9
RESEARCH PRODUCT
THE ROLE OF INFLAMMATION IN TYPE A AORTIC DISSECTION: A PILOT STUDY
Calogera PisanoEmiliano MaresiCesira PalmeriBalistrericarmela RitaGiovanni RuvoloGiuseppina CandoreTeresa D'amicosubject
Candidate genePathologymedicine.medical_specialtyImmunologylcsh:MedicineInflammationSingle-nucleotide polymorphismEnosmedicine.arterymedicineeNOsTAAD inflammation inflammatory molecules and genetic factors SNPs of ACE eNOs MMP-2-9 genesImmunology and AllergySettore MED/05 - Patologia ClinicaInflammatory molecules and genetic factorsAortic dissectionInflammationTAADAortabiologyMMP-2lcsh:RSettore MED/23 - Chirurgia Cardiacamedicine.diseasebiology.organism_classification-9 genesPathophysiologyeNOs; Inflammation; Inflammatory molecules and genetic factors; MMP-2-9 genes; SNPs of ACE; TAAD; Immunology and Allergy; ImmunologyTLR4SNPs of ACEmedicine.symptomdescription
Type 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.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2013-01-01 |