Detection of human apolipoprotein B polymorphic species with one monoclonal antibody (BIP 45) against low density lipoprotein influence of this polymorphism on lipid levels and coronary artery stenosis

• Published in: Atherosclerosis Vol. 66; no. 1; pp. 153 - 161
• Main Authors: Duriez, P., Vu Dac, N., Koffigan, M., Puchois, P., Demarquilly, C., Fievet, C., Fievet, P., Luyeye, I., Bard, J.M., Fourrier, J.L., Shmane, N., Lablanche, J.M., Bertrand, M., Fruchart, J.C.
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier Ireland Ltd 01.07.1987; Elsevier
• Subjects: Animals; Antibodies, Monoclonal - immunology; Apo B epitopes; Apo B polymorphism; Apolipoproteins B - genetics; Applied sciences; Coronary artery disease; Coronary Disease - genetics; Exact sciences and technology; Familial hypercholesterolemia; Lipids - blood; Lipoproteins, LDL - immunology; Male; Mice; Other techniques and industries; Polymorphism, Genetic; Apo B polymorphism; Apo B epitopes; Familial hypercholesterolemia; Coronary artery disease
• ISSN: 0021-9150; 1879-1484
• DOI: 10.1016/0021-9150(87)90191-2

The immunoreactivity of apolipoprotein B (apo B) in plasma samples obtained from a variety of subjects was analysed by non-competitive ELISA with a polyclonal and a monoclonal (BIP 45) anti-LDL antibody. Three populations were tested: the first, comprising 244 healthy male volunteers, provided reference values; the second consisted of a population undergoing coronary angiography (n = 88) and was divided into a subgroup with (n = 64) and without (n = 24) coronary artery disease (CAD); the third was made up of 56 patients with heterozygous familial hypercholesterolemia. Total apo B (measured with the polyclonal antibody) was increased in the populations with CAD and in the heterozygous familial hypercholesterolemic subjects compared to the reference population. When monoclonal antibody BIP 45 was used in the non-competitive ELISA, three different patterns emerged in each population, corresponding to weak, intermediate and strong binding of the particles containing apo B to the monoclonal antibody. This may result from genetic polymorphism of apo B, and in the reference population the data fit a model consisting of two co-dominant apo B alleles (BIP(-) and BIP(+)); the 3 subpopulations then correspond to the 2 homozygotes and the heterozygote. The number of patients whose particles bound weakly to monoclonal BIP 45 antibody was 'low in the CAD population, while intermediate binding was increased in this group. Nevertheless, when the analysis of variance of allele BIP(-) was studied no significant difference between groups was established. This finding indicates that the genetic difference in apo B detected by BIP 45 may not be significant in the development of CAD. Furthermore, the apo B genetic polymorphism detected by BIP 45 is not associated with a particular lipoprotein level in the reference population.