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Extracellular vesicles from epicardial fat mediate long-distance heart-brain communication and promote atrial fibrillation associated cognitive impairment (EAT exosomal miRNA-seq and hippocampal mRNA-seq)

ABSTRACT: 2 weeks of rapid atrial pacing increased the release of epicardial adipose tissue (EAT) exosomes. The red fluorescence of Ad-CD63-RFP traces the increase of EAT exosomes in the canine hippocampus. RNA Sequencing showed that the differentially expressed genes of cfa-miR-22e in EAT exosomes were significantly increased, and its target gene of IL33 was down-regulated in the hippocampus. Exosomes secreted by EAT in AF model canine penetrate the BBB, and activate hippocampal microglia through cfa-miR-22e/IL33 signaling pathway, which may be related to the increased risk of cognitive impairment in AF.

ORGANISM(S): Canis lupus familiaris

PROVIDER: GSE240776 | GEO | 2024/05/01

REPOSITORIES: GEO

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Project description: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.

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Extracellular vesicles from epicardial fat mediate long-distance heart-brain communication and promote atrial fibrillation associated cognitive impairment (EAT exosomal miRNA-seq and hippocampal mRNA-seq)

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