Proteomics

Dataset Information

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EAT and coronary atherosclerosis in high-risk patients


ABSTRACT: Rationale: Epicardial adipose tissue (EAT) has been independently associated with non-calcified, high-risk coronary plaques in low-to intermediate risk subjects. Recently, a bidirectional communication was shown between EAT and diseased coronary arteries. In high-risk patients it is unknown whether quantitative measures of EAT can capture, and which molecular players are involved in this mutual interplay. Objective: In a high-risk population, we aimed to determine how the volume of EAT is linked to coronary artery disease (CAD) and to identify potential EAT-deregulated pathways in CAD patients specifically related to coronary artery calcification (CAC). Methods and Results: In a prospective cohort of 574 degenerative severe aortic stenosis patients referred to cardiac surgery, we quantified fat depots by computed tomography (CT) and performed a comparative quantitative proteomics of thoracic fat, including EAT, mediastinal (MAT) and subcutaneous (SAT) adipose tissues. We did not find an independent association of EAT volume with the severity, distribution and complexity of coronary stenosis in invasive coronary angiography. Although, EAT volume was correlated with high CAC, its cardiovascular risk factors-adjusted association was not significant. Taking as reference non-CAD matched-patients and compared to MAT and SAT, EAT proteomic signature of CAD was characterized by up-regulation of pro-calcifying annexins (Annexin A2, ANXA2), fatty acid binding transporters (FABP4) and inflammatory signaling proteins, and by down-regulation of fetuin-A and redox state regulatory enzymes. In EAT, ANXA2 regulation was positively correlated with CAC. EAT gene expression studies confirmed overexpression of ANXA2 and FABP4 in CAD, but no expression of FETUA was detected. Compared with non-CAD, fetuin-A circulating levels were higher in CAD, whereas no fetuin-A pericardial fluid differences were found. Conclusions: In this high-risk cohort, EAT presented an imbalance of pro-calcifying, pro-inflammatory and lipid transporters mediators. These local EAT-mediated regulatory mechanisms were not reflected by the CT volume of EAT alone.

INSTRUMENT(S): TripleTOF 5600

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Heart

DISEASE(S): Cardiovascular System Disease

SUBMITTER: Cátia Santa  

LAB HEAD: Bruno Manadas

PROVIDER: PXD008852 | Pride | 2022-03-04

REPOSITORIES: Pride

Dataset's files

Source:
Action DRS
S160310_EAT_1.wiff Wiff
S160310_EAT_1.wiff.scan Wiff
S160310_EAT_112.wiff Wiff
S160310_EAT_112.wiff.scan Wiff
S160310_EAT_118.wiff Wiff
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Publications

Epicardial adipose tissue volume and annexin A2/fetuin-A signalling are linked to coronary calcification in advanced coronary artery disease: Computed tomography and proteomic biomarkers from the EPICHEART study.

Mancio Jennifer J   Barros Antonio S AS   Conceicao Gloria G   Pessoa-Amorim Guilherme G   Santa Catia C   Bartosch Carla C   Ferreira Wilson W   Carvalho Monica M   Ferreira Nuno N   Vouga Luis L   Miranda Isabel M IM   Vitorino Rui R   Manadas Bruno B   Falcao-Pires Ines I   Ribeiro Vasco Gama VG   Leite-Moreira Adelino A   Bettencourt Nuno N  

Atherosclerosis 20191115


<h4>Background & aims</h4>The role of epicardial adipose tissue (EAT) in the pathophysiology of late stage-coronary artery disease (CAD) has not been investigated. We explored the association of EAT volume and its proteome with advanced coronary atherosclerosis.<h4>Methods</h4>The EPICHEART Study prospectively enrolled 574 severe aortic stenosis patients referred to cardiac surgery. Before surgery, EAT volume was quantified by computed tomography (CT). During surgery, epicardial, mediastinal (MA  ...[more]

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