Recombinant Human ST2s protein [His]

The ST2 gene (Growth stimulation expressed gene 2) occupies the 2q12 region of human chromosome 2 and covers a 40 kb stretch within the interleukin-1 receptor (IL-1R) superfamily. The ST2 gene generates four isoforms namely: transmembrane ST2 (ST2L), soluble ST2 (sST2), ST2V, and ST2LV. ST2L receptor functions through its extracellular domain that holds three immunoglobulin-like motifs then connects to a transmembrane segment which leads into an intracellular Toll/IL-1R (TIR) domain. Although the soluble ST2 isoform shares the extracellular domain of ST2L it lacks both transmembrane and intracellular portions which stops it from triggering intracellular signaling pathways. After secretion into the extracellular area, sST2 becomes measurable within serum. The expression of this protein occurs in mast cells and fibroblasts while cytokines such as TNF-α trigger its induction in endothelial cells and it becomes highly expressed in damaged or stressed cardiomyocytes as well as epithelial cells, smooth muscle cells, and microvascular endothelial cells. The elevation of sST2 levels demonstrates myocardial damage that occurs alongside inflammatory processes and immune system abnormalities.

The endogenous ST2L ligand IL-33 attaches to ST2L and then gathers IL-1RAcP to build a heterodimer which triggers downstream signaling cascades and enhances Th2 cytokine output. Research indicates that the IL-33/ST2L pathway contributes to cardiovascular system protection. Increased sST2 levels prevent IL-33-ST2L interaction which reduces cardiac protection and correlates strongly with heart failure (HF) severity and negative outcomes.

Figure 1. Interleukin-33/ST2L signaling
(Source: Mueller T, et al. 2015)

sST2, a novel biomarker, demonstrates unique advantages in HF diagnosis and prognosis: The concentration of sST2 remains constant regardless of age, renal function or body mass index while showing a positive association with the severity of left ventricular remodeling and fibrosis. Research indicates that using sST2 with NT-proBNP enhances acute HF risk prediction and allows real-time assessment of therapeutic effects. Heart failure patients with sST2 levels above 35 ng/mL exhibit a mortality risk that is 2.8 times greater over the next 12 months. The potential of sST2 extends to evaluating left ventricular remodeling following acute myocardial infarction and determining the stability of atherosclerotic plaques.

Human soluble ST2 protein
Human soluble Suppression of Tumorigenicity 2 protein
Human soluble Growth Stimulation Expressed Gene 2 protein