Nori Human ST2 ELISA Kit Summary

Alternative names for ST2: IL1RL1, interleukin 1 receptor-like 1, DER4

Q01638

Standard Curve

Kit Components
1. Pre-coated 96-well Microplate
2. Biotinylated Detection Antibody
3. Streptavidin-HRP Conjugate
4. Lyophilized Standards
5. TMB One-Step Substrate
6. Stop Solution
7. 20 x PBS
8. Assay Buffer

Other Materials Required but not Provided:
1. Microplate Reader capable of measuring absorption at 450 nm
2. Log-log graph paper or computer and software for ELISA data analysis
3. Precision pipettes (1-1000 µl)
4. Multi-channel pipettes (300 µl)
5. Distilled or deionized water

Protocol Outline
1. Prepare all reagents, samples and standards as instructed in the datasheet.
2. Add 100 µl of Standard or samples to each well and incubate 1 h at RT.
3. Add 100 µl of Working Detection Antibody to each well and incubate 1 h at RT.
4. Add 100 µl of Working Streptavidin-HRP to each well and incubate 20 min at RT.
5. Add 100 µl of Substrate to each well and incubate 5-30 min at RT.
6. Add 50 µl of Stop Solution to each well and read at 450 nm immediately.

Background: 

ST2 is a cardiac biomarker encoded by the IL1RL1 gene and is a member of the interleukin 1 receptor family.^[1] The ST2 has two isoforms and is directly implicated in the progression of cardiac disease: a soluble form (soluble ST2 or sST2) and a membrane-bound receptor form (ST2 receptor or ST2L). When the myocardium is stretched, the ST2 gene is upregulated, increasing the concentration of circulating soluble ST2. ST2 is also known as IL-33R since IL-33 is its ligand. Binding of IL-33 to ST2, in response to cardiac disease or injury, such as an ischemic event, elicits a cardioprotective effect resulting in preserved cardiac function. This cardioprotective IL-33 signal is counterbalanced by the level of soluble ST2, which binds IL-33 and makes it unavailable to ST2L for cardioprotective signaling. As a result, the heart is subjected to greater stress in the presence of high levels of soluble ST2. ST2 signals the presence and severity of adverse cardiac remodeling and tissue fibrosis, which occurs in response to myocardial infarction, acute coronary syndrome, or worsening heart failure. ^[2] ST2 is an active participant in the cardiac remodeling pathway and could identify which patients will respond to Eplerenone, or other therapies that reverse myocardial fibrosis.^[3]  ST2 production is stimulated by proinflammatory stimuli.^[4] ST2 provides prognostic information that is independent of other cardiac biomarkers such as BNP, NT-proBNP, highly sensitive troponin, GDF-15, and galectin-3. Studies have shown patients with ST2 levels above a clinical threshold consistently have a much higher risk of mortality while, equally important, patients with ST2 levels below threshold have a very low risk of mortality.^[5][6] Although it has been shown that ST2 concentrations correlate with heart failure severity^[7] there is no level that perfectly separates patients with and without heart failure for disease diagnosis. However, as a prognostic marker it has been clearly shown that patients are at a higher risk of adverse outcomes when ST2 levels are above a cutoff value of 35 ng/mL.^[5] ST2 is a strong predictor of cardiovascular death and risk of developing new heart failure in ST Elevation Myocardial Infarction (STEMI) & NSTE-ACS patients. In patients presenting with Acute Coronary Syndrome (ACS), those in the highest quartile (above 35 ng/ml) have more than 3 times higher risk of cardiovascular death and new heart failure at 30 days, than those in the lower quartiles.

References

1. Tominaga S, et al (1992) Biochim Biophys Acta 1171 (2), 215-218.
2. Rehman SU, et al. (2008). J. Am. Coll. Cardiol. 52(18): 1458–65.
3. Weir RA, et al. (2010). J Am Coll Cardiol. 55 (3): 243–50.
4. Kumar S, et al. (1997) Biochem Biophys Res Commun 235 (3), 474-478.
5. Ky B, et al. (2011). Circ Heart Fail. 4 (2): 180–7.
6. Kohli P, et al. (2011). Clin. Chem. 58 (1): 257–66.
7. Socrates T, et al. (2010). J. Intern. Med. 268(5): 493–500.