Figure 2 | Scientific Reports

Figure 2

From: Dysfunctional EAT thickness may promote maladaptive heart remodeling in CVD patients through the ST2-IL33 system, directly related to EPAC protein expression

Figure 2

ST2 and IL-33 cardiac stretch mediators expression, production and immunolocalization in EAT. Under biomechanical stretchING the main cytokines involved in compensatory remodeling in the heart are ST2 and IL-33. We measured their expression, protein production and total circulating levels in EAT biospies from CVD patients. (a) EAT presents significantly higher expression of IL-33 gene than IL1RL1 (ST2), and ST2 and IL-33 expression is inversely correlated. sST2 total circulating level is higher than Il-33 circulating protein. (b) Western blot shows that EAT is a source of the ST2 cardiac stretch mediator and IL-33 cardioprotective proteins. (c) Representative images of EAT biopsies with immunoreaction for ST2 and IL-33 positive cells in separate panels (panels II with magnification). Both ST2 immunoreactivity and IL-33 are present in EAT biopsies specially those close to endothelial vessels.

Back to article page