Category: Biomarker Spotlight

The mature form of brain natriuretic peptide (BNP) is formed from the BNP (1-108) precursor and is secreted predominantly by the cardiac ventricles. Circulating forms of BNP include BNP-32 (77-108), a high molecular weight BNP which has not been well characterized and and the nt-proBNP (1-76). The BNP fragment is typically measured as a proxy for BNP because of its longer half-life. Recent research suggests that natriuretic peptides are important protectors against fluid overload and high blood pressure. BNP has also been implicated as a valuable marker in assessing cardiac risk.

The natriuretic peptides are members of a family of structurally similar but genetically distinct peptide hormones, consisting of atrial-, brain-, and C-type (ANP, BNP, and CNP, respectively). ANP and BNP preferentially bind to a membrane-bound guanylyl cyclase (GC) receptor called GC-A or NPR1, whereas CNP is the physiological ligand for GC-B (NPR2). The natriuretic peptides play an important role in the regulation of cardiovascular and renal homeostasis and in the regulation of fatty acid metabolism and body weight.
BNP is mainly expressed by ventricular myocardium in response to volume overload and increased filling pressure. BNP has a cleavable signal sequence. Mature BNP consists of 108 amino acids (proBNP or BNP-108), and undergoes cleavage resulting in physiologically active BNP-32 and additional C-terminal fragments along with a physiologically inactive N-terminal peptide comprising amino acids 1-76, which is further degraded proteolytically. BNP fragments in the circulation are therefore very heterogenous.
BNP has a key role in cardiovascular homeostasis with biological actions including natriuresis, diuresis, vasorelaxation, and inhibition of renin and aldosterone secretion. A high concentration of BNP in the bloodstream is indicative of heart failure. The discovery of natriuretic peptides identified an endocrine system that contributes to diuresis and vascular tone. The biology, biochemistry and the pathophysiological role of natriuretic peptides are described in several reviews.

NT-proBNP ELISA Assay Kit

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Lipid peroxidation is a well-established mechanism of cellular injury in both plants and animals and is used as an indicator of oxidative stress in cells and tissues. Lipid peroxides are unstable and decompose to form a complex series of compounds including reactive carbonyl compounds. Polyunsaturated fatty acid peroxides generate malondialdehyde (MDA) and 4-hydroxyalkenals (HAE) upon decomposition. The measurement of MDA and HAE has been used as an indicator of lipid peroxidation (1).

A study was published in the journal Life Sciences, on the role vanillin plays as either prophylaxis or treatment in liver regeneration augmentation. Check out the full text here. 

Abstract

Aims
This study has been designed to investigate the role of vanillin either as prophylaxis or treatment in liver regeneration augmentation and liver fibrosis regression in thioacetamide (TAA) induced liver damage.

Materials and Methods
Animals were injected with TAA to induce liver injury (200 mg/kg twice weekly) for 8 weeks. In vanillin prophylaxis group; rats were administered vanillin (100 mg/Kg; IP, daily) from day 1 of TAA injection for 8 weeks. In vanillin treatment group; rats were confronted with the same dose of TAA injection for 8 weeks then treated with vanillin (100 mg/Kg, IP, daily) for 4 weeks. ALT, AST activities, serum albumin, hepatic GSH, MDA, HGF, VEGF, IL-6 and TNF-α levels were measured and also, MMP-2, TIMP-1 and cyclin D gene expression were determined. Liver sections were stained with H&E and Sirius red and immunostained for Ki-67 and α-SMA for histological and immunohistological changes analysis.

Key Findings
Vanillin improved liver function and histology. Also, showed a remarkable increase in hepatic HGF and VEGF level, and up-regulation of cyclin D1 expression accompanied by a significant up-regulation of MMP-2 and down- regulation of TIMP-1. All these effects were accompanied by TNF-α, IL-6 and oxidative stress significant attenuation.

Significance
In conclusion, vanillin enhanced liver regeneration in TAA-induced liver damage model; targeting growth factors (HGF, VEGF) and cellular proliferation marker cyclin D1. As well as stimulating fibrosis regression by inhibition of ECM accumulation and enhancing its degradation.

About the Lipid Peroxidase Assay

Sample Type: Biological Fluids
Sample Size: 140 µl
Incubation Time: 3 hours

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The Secretory Leukocyte Peptidase Inhibitor Protein (SLPI) is a secreted inhibitor that protects epithelial tissues from serine proteases. It is found in various secretions including seminal plasma, cervical mucus, and bronchial secretions, and has an affinity for trypsin, leukocyte elastase, and cathepsin G. Its inhibitory effect contributes to the immune response by protecting epithelial surfaces from attack by endogenous proteolytic enzymes. The SLPI protein is also thought to have broad-spectrum antibiotic activity.

SLPI has been known by many names, including Antileukoproteinase protein, ALP Protein, ALK1 protein, BLPI protein, HUSI protein, HUSI-I protein, MPI protein, WAP4 protein, WFDC4 protein.

A study was published from Acta Biomaterialia, on oral junctional epithelium for surface-mediated soft tissue attachment to prevent failure of percutaneous devices.  Check out the full text article here.

Abstract

Teeth, long-lasting percutaneous organs, feature soft tissue attachment through adhesive structures, hemidesmosomes, in the junctional epithelium basement membrane adjacent to teeth. This soft tissue attachment prevents bacterial infection of the tooth despite the rich – and harsh – microbial composition of the oral cavity. Conversely, millions of percutaneous devices (catheters, dental, and orthopedic implants) fail from infection yearly. Standard of care antibiotic usage fuels antimicrobial resistance and is frequently ineffective. Infection prevention strategies, like for dental implants, have failed in generating durable soft tissue adhesion – like that seen with the tooth – to prevent bacterial colonization at the tissue-device interface. Here, inspired by the impervious natural attachment of the junctional epithelium to teeth, we synthesized four cell adhesion peptide (CAPs) nanocoatings, derived from basement membranes, to promote percutaneous device soft tissue attachment. The two leading nanocoatings upregulated integrin-mediated hemidesmosomes, selectively increased keratinocyte proliferation compared to fibroblasts, which cannot form hemidesmosomes, and expression of junctional epithelium adhesive markers. CAP nanocoatings displayed marked durability under simulated clinical conditions and the top performer CAP nanocoating was validated in a percutaneous implant murine model. Basement membrane CAP nanocoatings, inspired by the tooth and junctional epithelium, may provide an alternative anti-infective strategy for percutaneous devices to mitigate the worldwide threat of antimicrobial resistance.

About the SLPI Protein ELISA Assay

• Sample Size – 50 µL
• Sample Type – Serum
• Incubation Time – 2.5 hours

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Vanin-1 (VAN1) is an anchored protein that catalyzes the hydrolysis of pantetheine to pantothenic acid (vitamin B5) and cyteamine. VAN1 has a broad tissue expression with the highest levels being observed in kidney tubular epithelial cells. The GPI anchor of VAN1 can be cleaved by a yet unknown mechanism, resulting in VAN-1 being shed into the extracellular space.

Vanin-1 plays a pivotal role in oxidative stress and the inflammatory response. However, its relationship with traumatic sepsis remains unknown. In a study aimed to identify whether VAN1 could be used as a biomarker for traumatic sepsis, scientists found there is a significant relationship between plasma VAN1 and sepsis in both the internal test cohort and the external validation cohort. These results contribute to the body of evidence supporting the use of plasma VAN1 in the early prediction of traumatic sepsis.

Learn more about that study here.

Eagle Biosciences offers a comprehensive Vanin-1 ELISA for urine samples.

Vanin-1 ELISA Assay Highlights

• Optimized for human urine samples
• Highly SPECIFIC and DEFINED characterized antibodies
• RELIABLE – rigorously validated
• QUICK one-step ELISA

We also provide a Vanin-1 Mouse/Rat ELISA Assay Kit that has been validated for mouse or rat serum, plasma, or urine samples.

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Pentraxins are a superfamily of acute phase reactants characterized by a pentameric structure. Pentraxin 3 (PTX3), is locally produced and released by a variety of cell types including macrophages, neutrophils, myeloid-derived mesangial cells, synovial cells, smooth muscle cells, alveolar epithelium, and glial cells. PTX3 is induced in response to either inflammatory cytokines interleukin-1 β (IL-1 β) and tumor necrosis factor α (TNFα) or the selected associated molecular patterns (PAMPs). PTX3 is elevated in critically ill patients, with a gradient from systematic inflammatory response syndrome to septic shock, and in several other diseases, such as myocardial infarction, rheumatoid arthritis, atherosclerosis, small vessel vasculitis and psoriasis.

Oncologists at Queen Mary’s University whether PTX 3 could be a reliable biomarker for detection of pancreatic ductal adenocarcinoma (PDAC). PDAC is characterized by an intense desmoplastic stroma, laid down by the pancreatic stellate cells (PSC). One of the defining features of PDAC is that there are very few cancer cells. Pancreatic cancer is surprisingly made up of mostly non-cancer cells, which have been co-opted by cancer to build a huge amount of scar tissue or stroma around the cancer, providing a strong defense for the cancer cells. The researchers found that PTX3 is a putative stromally-derived biomarker for PDAC which warrants further testing in prospective, larger, multi-center cohorts and within clinical trials targeting stroma.

To read more about this study, click here.

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Endostatin, a 20-kDa C-terminal proteolytic fragment of collagen XVIII, is an endogenous angiogenesis inhibitor localized in the vascular basement membrane in various organs. The biological functions of the endostatin-network involve SPARC, thrombospondin-1, glycosaminoglycans, collagens, and integrins. It is expressed during the progression of renal fibrosis in tubular cells of injured tissue. In renal micro-vascular disease, observed in late stages of patients with chronic kidney disease, increased endostatin levels are possibly the consequence of enhanced extracellular matrix degradation. Thus, it may become an important marker for progressive microvascular renal disease in patients with chronic kidney disease. Endostatin levels in blood are also likely to increase in patients with other microvascular tissue injuries, including atherosclerosis, myocardial- and brain ischemia. In ischemic stroke patients, high endostatin plasma levels predict a worse long-term clinical outcome.

A team of researchers recently demonstrated that serial measurement of endostatin in plasma has useful predictive value for 30-day mortality in Acute Kidney Injury (AKI) patients after major surgery.

Prognostic value of dynamic plasma endostatin for the prediction of mortality in acute kidney injury: A prospective cohort study. Jia HM et al., J Int Med Res. 2020 48(7):300060520940856.. Full Text.

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Endostatin ELISA Assay Kit

A recent systemic review and meta-analysis of studies with serum amyloid A in patients with COVID-19 published by the International Journal of Infectious Diseases has found high concentrations of serum amyloid A associated with higher COVID-19 severity and mortality. This review analyzed nineteen studies consisting of over five thousand patients with COVID-19. The pooled results showed that serum amyloid A concentrations were significantly higher in those patients with severe disease and non-survivors. This measurement could be useful for risk stratification and clinical monitoring of these patients.

Background

A state of excessive local and systemic inflammation and immune activation are strongly associated with oxidative stress, coagulation abnormalities, and multi-organ dysfunction in patients with coronavirus disease 2019 (COVID-19). While safe and effective vaccines have been developed and are currently being rolled out, effective therapies to mitigate the clinical manifestations of COVID-19, e.g., repurposed antiviral and immunosuppressant agents, remain limited. In this context, the use of biomarkers of disease severity and clinical progression would facilitate the early identification of patients requiring aggressive management and monitoring and assist with the judicious use of healthcare resources. Given the key pathophysiological role of inflammation and immunity in the clinical progress of COVID-19, markers that reflect the activation of these pathways might be particularly useful for risk stratification and effective management.

Serum amyloid A (SAA) genes and proteins are significantly activated during the acute phase response, which comprises a number of phenomena that occur in the presence of inflammation and infection, e.g., increased temperature and hormonal and metabolic alterations. Circulating SAA concentrations, typically low under physiological circumstances (20–50 mg/l), can increase up to 1000-fold within the first 24–48 h of an acute phase response. This is the consequence of increased synthesis in the liver that is triggered by several stimuli, including tumor necrosis factor (TNF), interleukin (IL)-1β, IL-6, and interferon gamma (IFN-γ). SAA, in turn, can activate the complement system and the nucleotide-binding domain leucine-rich repeat-containing family pyrin-domain containing 3 (NLRP3) inflammasome, further increase the synthesis of TNF, IL-1β, and IL-6, and activate other proinflammatory cytokines such as IL-1α and IL-23. Notably, these mediators have been shown to contribute significantly to the onset of the cytokine storm and its adverse clinical consequences in COVID-19. Therefore, it is plausible that the acute increase in SAA concentrations in patients with COVID-19 might not only reflect the presence of an acute phase response, but also herald the development of a cytokine storm and, consequently, multi-organ failure and an increased risk of adverse outcomes.

Two systematic reviews and meta-analyses on a relatively limited number of studies, three and five, respectively, have reported a significant and positive association between SAA concentrations and COVID-19 severity. Following the publication of several additional studies, an updated systematic review and meta-analysis was conducted of the available evidence on the clinical implications of SAA concentrations in patients with COVID-19.

Read the full text here.

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Sclerostin is a secreted glycoprotein that functions as a potent inhibitor of Wnt signaling. It acts by binding to the Wnt-coreceptor LRP5/6 thus inhibiting bone formation by regulating osteoblast function and promoting osteoblast apoptosis. Sclerostin is primarily produced by osteocytes. It inhibits the canonical Wnt pathway and thereby osteoblasts. It also stimulates RANKL release by the osteocytes and thereby osteoclast recruitment. Inhibition of sclerostin causes stimulation of bone formation and inhibition of resorption. Read more about sclerostin’s role in bone remodeling here.

Sclerostin levels are altered in response to hormonal stimuli or due to pathophysiological conditions. The concentrations are increased in disorders such as hypoparathyroidism, Paget’s disease, multiple myeloma and in cancer induced bone diseases. Mutations in the SOST gene can cause sclerosteosis and van Buchem disease which are bone dysplasia disorders characterized by progressive skeletal overgrowth. Sclerostin levels are decreased in primary hyperparathyroidism, as well as by the mechanical stimulation of bone.

A mini-review was published in the The Journal of Clinical Endocrinology & Metabolism regarding the effect of sclerostin inhibition on the cardiovascular safety of patients. Read the full text here.

Eagle Biosciences offers a sensitive and reliable assay for the detection of sclerostin in serum and plasma samples.

Advantages of the Sclerostin ELISA Assay Kit

• • High Quality – rigorously validated according to ICH/FDA/EMEA guidelines
  • Low Sample Volume – only 20ul of sample per well
  • Easy – ready to use protocol, standards and controls included

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Receptor activator of nuclear factor kappa B ligand, RANKL, and its specific receptor RANK, are members of the tumor necrosis factor (TNF) family and are the main stimulatory factor for the formation of mature osteoclasts and are essential for their survival. The major source of RANKL are osteocytes, former osteoblasts that become embedded within the mineralized bone matrix. RANKL and its specific receptor RANK are not only key regulators of bone remodeling but also play an essential role in immunobiology, e.g. lymph node formation, establishment of the thymic microenvironment, mammary gland development during pregnancy, bone metastasis in cancer and sex-hormone, progestin-driven breast cancer, thermoregulation, and finally in the development of type 2 diabetes mellitus.

A recent study has uncovered a new role for RANKL and RANK in bone remodeling. Researchers have found that extracellular vesicles containing RANKL and RANK may have an important role in the long range signaling for bone remodeling. These signaling molecules have the potential to be targeted for therapeutics and also used diagnostically.

Click here to learn more.

Holliday LS, Patel SS, Rody WJ. RANKL and RANK in Extracellular Vesicles: Surprising New Players in Bone Remodeling. Extracell Vesicles Circ Nucleic Acids. 2021; 2:18-28.

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