Study of the expression of the genetic variants of XXXX alpha1-acid glycoprotein in healthy subjects using isoelectric focusing and immunoblotting.

@entity1 @entity32 @entity5 @entity5064 @entity70729
@entity1 alpha1-acid glycoprotein (AAG) exists as an heterogeneous population of two or three genetic variants ( @entity5064 F1 and/or S and @entity70729 A) in the plasma of most individuals. The @entity5064 and @entity70729 variants have a separate genetic origin. AAG belongs to the acute-phase proteins, which, under conditions of @entity32 , increase several-fold in concentration. Additionally, there is evidence to suggest that it is not only the concentration but also the distribution of the two gene products of AAG ( @entity5064 and @entity70729 ) that alter in such conditions. Variations of the relative concentrations of the AAG variants in certain diseases, such as @entity5 , can only be shown by reference to data collected in healthy @entity1 . In this study, we have investigated a group of 74 healthy subjects (42 @entity1 and 32 @entity1 ) for AAG concentrations, AAG phenotypes and relative proportions of genetic variants in plasma. The specific assay of AAG was carried out by an immunonephelometric method and the phenotyping was performed, after desialylation of AAG, by analytical isoelectric focusing. Detection of the AAG variants was made by immunoblotting and their relative proportions were determined by laser densitometry analysis. The AAG plasma concentrations in the healthy group ranged between 0.28 and 0.92 g/l (mean value 0.50+/-0.14 g/l). The relative proportions of the variants derived from the two genes of AAG were variable, depending on the individual, but the amount of @entity5064 variants almost always exceeded that of the @entity70729 variant. No sex-related differences were observed in respect either in the total AAG level nor the relative proportions of the @entity5064 and @entity70729 variants. The data collected in this study may serve as a reference towards the investigation of possible changes in the expression of the genetic variants of AAG in chronic inflammatory diseases.
