Get a Quote
| Name | Anti-Human Brain natriuretic peptide (BNP) antibody | |||
| Platforms | Chemiluminescence immunoassay (CLIA) Immunochromatography assay (ICA) |
|||
| Catalog # | K136m1 | R195e5 | ||
| Usage | Detection/Capture | Detection/Capture | ||
| Description | Monoclonal antibody, cultured in vitro | |||
| Buffer | 1×PBS | |||
| Purity | Purity>98%, purified by Protein A/G chromatography | |||
| Storage | Aliquot and store at -20°C or lower. Avoid freeze / thaw cycles. | |||
| Name | Pro-Brain natriuretic peptide (BNP) antigen | |||
| Description | Recombinant, C-terminal His-tagged, in vitro expressed from mammalian cells | |||
| Applications | Calibrator and quality control product | |||
| Catalog # | C1536 | |||
| Purity | >90%, analyzed by R250-stained SDS-PAGE | |||
| Buffer | 1x PBS，pH 7.4 | |||
| Storage | Aliquot and store at -80°C. Avoid freeze / thaw cycles. | |||
| SDS-PAGE |
Predicted MW around 20-25kDa (tagged)
|
|||
When the transmural response of cardiomyocytes increases, ProBNP is released and cleaved into active BNP and inactive N-terminal pro-BNP (NT-ProBNP). BNP eventually binds to the natriuretic peptide C receptor (NPR-C) and is subsequently degraded by endocytosis and lysosome.
The concentration of BNP increases significantly with the elevation of ventricular pressure when cardiac dysfunction happens. The concentration of BNP decreases significantly after heart failure patients accepting treatments for 12 hours. Therefore, BNP can be used as an independent predictor of the prognosis of heart failure and myocardial infarction, or dynamically monitoring the treatment effect of heart failure patients. It is the "gold standard" for the diagnosis of heart failure in the emergency room.
BNP reference value (ESC guidelines for the diagnosis of heart failure) :
| BNP< 100pg/mL | Heart failure was basically excluded, negative accuracy up to 97.7% |
| 100pg/ml< BNP< 400pg/ml | Barely diagnosed |
| BNP >400pg/ml | Potential heart failure |
Myocardial ischemia can trigger the release of many endogenous cytoprotective factors such as BNP. In rat cardiac model of acute myocardial infarction, exogenous BNP is able to limit the infarct size in a concentration-dependent manner, which is an endocrine-independent cytoprotective effect of the peptide.
The mechanism of this acute protective effect of BNP appears to be related to the increased conversion of the second messenger guanosine triphosphate to cyclic guanosine monophosphate (cGMP), which also involves the opening of mitochondrial ATP-sensitive potassium (KATP) channels. Many endogenous protective mediators are considered to act on G protein-coupled receptor to perform anti-ischemic effects through the opening of mitochondrial KATP channels. In some cardiac diseases, G protein-coupled receptor responses may be downregulated. At this time BNP adopts a novel molecular signaling pathway, in which BNP/NPR-A induces cGMP to increase and activates cGMP-dependent protein kinase-I (cGK-I), through The cGMP/cGK-I pathway to open the KATP channel. Therefore, the BNP/NPR-A signaling pathway can be reserved as a very effective rescue pathway to protect and rescue the tissue.
The expression of myocardial BNP continues to increase and affects tissue remodeling after myocardial infarction happens, which may be related to the inhibition of BNP on fibroblast activity and cardiomyocyte hypertrophy. Research indicates that BNP and atrial natriuretic peptide (ANF) have obvious effects on cardiac fibroblasts. Both of these peptides inhibit in vitro synthesis of collagen in cardiac fibroblasts during hypoxia and inhibit the proliferation of fibroblast upon stimulated by angiotensin II. Meanwhile, multifocal cardiac fibrosis was found in mice lacking of BNP. What’s more, NPR-A-/- knockout mice may also develop hypertension along with myocardial hypertrophy and fibrosis.
In summary, brain natriuretic peptide (BNP) is a pleiotropic peptide, which has important clinical and therapeutic significance for asymptomatic left ventricular dysfunction, heart failure, acute ischemia, myocardial infarction and other cardiac diseases.
References
[1] Weber M, Hamm c. Role of B-type natriuretic peptide (BNP) and NT-proBNP in clinical routine[J]. Heart, 2006, 92(6):843.
[2] O Nakagawa, Y Ogawa, H Itoh, et al. Rapid transcriptional activation and early mRNA turnover of brain natriuretic peptide in cardiocyte hypertrophy. Evidence for brain natriuretic peptide as an "emergency" cardiac hormone against ventricular overload[J]. J. Clin. Invest,1995,96:1280-1287.
[3] Redfield M M, Rodeheffer R J, Steven J Jacobsen MD, et al. Plasma brain natriuretic peptide concentration: impact of age and gender.[J]. Joumal of the American College of Cardiology, 2002, 40( 5):976-982.
[4]S,P,D' Souza, et al. B Type natriuretic peptide: a good omen in myocardial ischaemia?[J]. Heart Official Journal of the British Cardiac Society, 2003:707-709.
