Anti-A2M monoclonal antibody, clone G2-Q2D22#4 (3O2/20)

The aims of this study were to investigate transplacental transport of alpha2-macroglobulin (alpha2M) in rats and to examine the degree of a2M induction in maternal and neonatal rats with acute inflammation. Serum was collected from healthy pregnant CD (IGS) rats, neonates of the pregnant rats and their cord blood. Additional serum samples were obtained from pregnant rats inoculated with an inflammatory agent, turpentine oil, their neonates and cord blood, and neonates inoculated with turpentine oil. The serum levels of alpha2M were measured by means of an enzyme-linked immunosorbent assay. The average serum levels of alpha2M in healthy neonates and cord blood were about 380 mug/ml. Serum alpha2M level in neonates inoculated with turpentine oil averaged about 580 mug/ml. Serum alpha2M levels in maternal rats inoculated with turpentine oil, neonates from those rats and their cord blood were elevated, the values being 2,000 mug/ml or higher. It was demonstrated that induction of alpha2M in neonatal rats was lower than in maternal rats when inoculated with turpentine oil. These results suggest that alpha2M is transplacentally transported from maternal rats to fetal ones.

alpha 2-macroglobulin (alpha(2)M) is an abundant plasma protein similar in structure and function to a group of proteins called alpha-macroglobulins. alpha(2)M is also produced in the brain where it binds multiple extracellular ligands and is internalized by neurons and astrocytes. In the brain of Alzheimer's disease (AD) patients, alpha(2)M has been localized to diffuse amyloid plaques. alpha(2)M also binds soluble beta-amyloid, of which it mediates degradation. However, an excess of alpha(2)M can also have neurotoxic effects. Based on genetic evidence, is now recognized as one of the two confirmed late onset AD genes. As for the three early onset genes (the amyloid beta-protein precursor and the two presenilins) and for the other late onset gene (ApoE), DNA polymorphisms in the A2M gene associated with AD result in significantly increased accumulation of amyloid plaques in AD brains. These data support an important role for A2M in AD etiopathology. (C) 2000 Published by Elsevier Science Inc.