Description

Genorise Recombinant Human Myeloperoxidase Protein Summary

Alternative names for myeloperoxidase: MPO

Product Specifications

Background: 

Myeloperoxidase (MPO) is a member of the XPO subfamily of peroxidase that in humans is encoded by the MPO gene on chromosome 17. MPO is most abundantly expressed in neutrophil granulocytes and is a lysosomal protein stored in azurophilic granules of the neutrophil and released into the extracellular space during degranulation.^[1] It produces hypohalous acids to carry out their antimicrobial activity. It requires heme as a cofactor. Furthermore, it oxidizes tyrosine to tyrosyl radical using hydrogen peroxide as an oxidizing agent.^[2] Hypochlorous acid and tyrosyl radical are cytotoxic, so they are used by the neutrophil to kill bacteria and other pathogens.^[3] However, this hypochlorous acid may also cause oxidative damage in host tissue. Moreover, MPO oxidation of apoA-I reduces HDL-mediated inhibition of apoptosis and inflammation.^[4] In addition, MPO mediates protein nitrosylation and the formation of 3-chlorotyrosine and dityrosine crosslinks. Recent studies have reported an association between elevated myeloperoxidase levels and the severity of coronary artery disease.^[5] And Heslop et al. reported that elevated MPO levels more than doubled might increase the risk for cardiovascular mortality over a 13-year period.^[6] It has also been suggested that myeloperoxidase plays a significant role in the development of the atherosclerotic lesion and rendering plaques unstable.^[7] MPO could serve as a sensitive predictor for myocardial infarction in patients presenting with chest pain.^[8] The 2010 Heslop et al. study reported that measuring both MPO and CRP provided added benefit for risk prediction than just measuring CRP alone.^[6]

References

1. Kinkade JM, et al. (1983). Biochem Biophys Res Communications. 114 (1): 296–303.
2. Heinecke JW, et al. (1993). The Journal of Clinical Investigation. 91 (6): 2866–72.
3. Hampton MB, et al. (1998). Blood. 92 (9): 3007–17.
4. Shao B, et al. (2010). Chemical Research in Toxicology. 23 (3): 447–54.
5. Zhang R, et al. (2001). JAMA. 286 (17): 2136–42.
6. Heslop CL, e tal. (2010). J American College of Cardiology. 55 (11): 1102–9.
7. Nicholls SJ, et al. (2005). Arteriosclerosis,Thrombosis and Vascular Bio. 25: 1102–11.
8. Brennan ML, et al. (2003). The New England Journal of Medicine. 349 (17): 1595–604.