Disease relevance of Mapre3

• METHODS: We evaluated the effects of depletion of circulating neutrophils by administration of an antineutrophil monoclonal antibody (RP3) on brain edema formation, infarct size, and neutrophil infiltration (myeloperoxidase [MPO]-quantified) in rats with 1 hour of middle cerebral artery (MCA) occlusion [1].
• Use of a transfection method to demonstrate a monolayer cell transforming agent from the EB3 line of Burkitt's lymphoma cells [2].
• RP3 treatment inhibited the neutrophil leukocytosis associated with AA (3.3 +/- 0.6 x 10(3)/mm3 versus 21.2 +/- 6.9 x 10(3)/mm3; P<0.001) [3].
• Specific anti-neutrophil MoAb, RP3 (10 mg), or a control antibody was given twice daily on days 8-11 after injection of Mycobacterium tuberculosis in inbred male Sprague-Dawley rats [3].
• Treatment with RP3 selectively and sufficiently depleted the circulating neutrophil population, markedly reduced MPO, and significantly attenuated LPO and the tissue water content after both 3- and 5-hr of ischemia [4].

High impact information on Mapre3

• Since APCL is also expressed highly and specifically in the central nervous system, APCL-EB3 interaction may be specific to the CNS, possibly involving stability and/or extension of microtubules during neuritogenesis [5].
• To study the role of neutrophils in radical production during cerebral ischemia-reperfusion, we evaluated the effects of depletion of circulating neutrophils by administration of an anti-neutrophil monoclonal antibody (RP3) on radical formation in rats with 1-h middle cerebral artery (MCA) occlusion [6].
• RP3 treatment exerted no effect on the changes in extracellular ascorbate or tissue PO2 throughout the experimental period [6].
• The expression of three proteins of pI/Mr x 10(-3) 5.9-7.2/205 (RP1), 6.5-7.5/160 (RP2) and 4.0/85 (RP3) consistently matched the transformed phenotype [7].
• Primary human amnion cell monolayers which had been treated with DEAE-dextran, washed, and then inoculated with sonicated cells of the EB3 line of Burkitt's lymphoma cells developed foci of transformed amnion cells 7 to 14 days later [2].

Anatomical context of Mapre3

• Depletion of neutrophils by RP3 treatment completely inhibited the increase in MPO activity in the ischemic brain after 24 hours of reperfusion [1].

Associations of Mapre3 with chemical compounds

• Cyclophosphamide induced marked neutropaenia whereas RP3 inhibited the neutrophilia observed after HgCl2 injection [8].

Analytical, diagnostic and therapeutic context of Mapre3

• However, RP3 treatment completely inhibited the increase in extracellular AR after reperfusion [6].

References