Project description:To better characterize the role of PCAT in the pathogenesis of disease, we performed a large-scale unbiased analysis of the transcriptional differences between pericardial and subcutaneous adipose tissue, analysing 53 microarrays across 19 individuals. Patients who underwent elective coronary artery bypass grafting and/or cardiac valve replacement surgeries participated in the study. Pericardial adipose tissue and subcutaneous adipose tissue were harvested from patients.
Project description:To better characterize the role of whole pericardial adipose tissue (PCAT) in the pathogenesis of disease, we performed a large-scale unbiased analysis of the transcriptional differences between pericardial and subcutaneous adipose tissue, analysing 53 microarrays across 19 individuals.
Project description:Mesenchymal stem/stromal cells (MSCs) were harvested from subcutaneous adipose tissue of patients with obesity or healthy controls and expanded for 3-4 passages, and 5hmC profiles were examined through hydroxymethylated DNA immunoprecipitation sequencing (hMeDIP-seq). We hypothesized that obesity and cardiovascular risk factors induce functionally-relevant, locus-specific changes in overall exonic coverage of 5hmC in human adipose-derived MSCs.
Project description:Visceral adiposity is a risk factor for severe COVID-19 and a link between adipose tissue infection and disease progression has been proposed. Here we demonstrate that SARS-CoV-2 undergoes productive infection in adipocytes, although the degree of infection and the cellular response depend on the anatomical origin of the adipocyte and the viral strain. Differentiated adipocytes from human visceral adipose tissue are more permissive to SARS-CoV-2 infection than their subcutaneous counterpart, and this associates with ACE2 expression. Infection of subcutaneous adipocytes leads to inhibition of lipolysis, while infection of visceral adipocytes results in higher expression of pro-inflammatory cytokines. Infected adipocytes begin to die 4 days after infection, regardless of the origin. The viral load and cellular response are attenuated when adipocytes are infected with the SARS-CoV-2 variant P.1. Hence, SARS-CoV-2 infects and replicates in adipocytes, where it compromises cell viability and alters lipid metabolism or elicits a pro-inflammatory response depending on the fat depot and the viral strain.
