Cardiovascular Risk Factors and Differential Transcriptomic Profile of the Subcutaneous and Visceral Adipose Tissue and Their Resident Stem Cells

Abstract

Background: The increase in the incidence of obesity and obesity-related cardiovascular risk factors (CVRFs) over the last decades has brought attention on adipose tissue (AT) pathobiology. The expansion of AT is associated with the development of new vasculature needed to perfuse the tissue; however, not all fat depots have the same ability to induce angiogenesis that requires recruitment of their own endothelial cells. In this study we have investigated the effect of different CVRFs, on the angiogenic capacity of the subcutaneous (SAT) and visceral (VAT) adipose tissue and on the function of their mesenchymal cell reservoir. Methods: A transcriptomic approach was used to compare the different angiogenic and inflammatory profiles of the subcutaneous and visceral fat depots from individuals with obesity, as well as their resident stem cells (ASCs). Influence of other risk factors on fat composition was also measured. Finally, the microvesicles (MVs) released by ASCs were isolated and their regenerative potential analyzed by molecular and cellular methodologies. Results: Obesity decreases the angiogenic capacity of AT. There are differences between SAT and VAT; from the 21 angiogenic-related genes analyzed, only three were decreased in SAT compared with those decreased in VAT. ASCs isolated from both fat depots showed significant differences; there was a significant up-regulation of the VEGF-pathway on visceral derived ASCs. ASCs release MVs that stimulate endothelial cell migration and angiogenic capacity. Conclusions: In patients with obesity, SAT expresses a greater number of angiogenic molecules than VAT, independent of the presence of other CVRFs.

Visceral adiposity index and atherogenic index of plasma as useful predictors of risk of cardiovascular diseases: evidence from a cohort study in Iran

“…In a meta-analysis study (2020), simple anthropometric indices including waist circumference (WC), body mass index (BMI), and waist to hip ratio (WHR) were introduced as acceptable predictors of CVDs [ 6 ]. However, these indices cannot measure visceral and subcutaneous fat, while visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) have an important role in pathogenesis of CVDs [ 7 , 8 ]. VAT can be evaluated using abdominal MRI (magnetic resonance imaging) or computed tomography (CT) scan; but these methods are expensive and limited and are not used for screening in large populations [ 8 ].…”

The Effects of Shear Force-Based Processing of Lipoaspirates on White Adipose Tissue and the Differentiation Potential of Adipose Derived Stem Cells

“…In addition to the improved mechanical properties, the completely processed lipoaspirates (after C2) has two other advantages. The increased number of SVCs and thus endothelial cells leads to the improved neoangiogenesis of the implanted tissue [ 27 , 28 , 29 ] and the smaller particle size after homogenization reduces the diffusion distance, resulting in better take rates and less necrosis [ 30 ]. It should be noted that the increase in SVCs ( Figure 4 a) results from the volume loss of adipocyte depots ( Figure 1 and Figure 3 ) and not from cell proliferation [ 14 ].…”

Diabetic cardiomyopathy: the need for adjusting experimental models to meet clinical reality

“…33,34 Overall, the mechanisms by which adiposity contributes to cardiac alterations largely overlap with those reported for diabetic CM and include oxidative stress, inflammation, apoptosis, dysregulated autophagy, hypertrophy, interstitial fibrosis, lipotoxicity and metabolic defects. It seems that not only the degree of adiposity counts but the location of body fat accumulation influences the risk of cardiac dysfunction: ectopic adiposity (visceral, pericardial and epicardial) carries a higher risk than subcutaneous fat 35,36 through the release of pro-inflammatory and pro-fibrotic factors. 37,38 Interestingly, the effects of HFD on cardiac remodelling are reversible, as a switch from HFD to standard diet for 8 weeks reduced lipid accumulation, myocardial hypertrophy, and fibrosis, and improved myocardial function in 16-week HFD mice.…”