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Journal of Lipid Research, Vol 35, 263-270, Copyright © 1994 by Lipid Research, Inc.
ARTICLES |
C Doucet, T Huby, J Chapman and J Thillet
Institut de la Sante et de la Recherche Medicale, Unite U321, Hopital de la Pitie Paris, France.
Several studies have documented the presence of Lp[a] in nonhuman primates. However, data are lacking in great apes such as the chimpanzee. We have studied the quantitative distribution of Lp[a], as well as the frequency of apo[a] phenotypes, in a population of chimpanzees living in Gabon. Monoclonal antibody 14A12, directed against human apo[a], failed to recognize chimpanzee Lp[a]. Therefore, Lp[a] was assayed using an ELISA involving two polyclonal antibodies, an anti-human apo[a] and an anti-human apoB-100. Under these conditions, Lp[a] was detected in each of 28 animals. The plasma level of Lp[a] was found to be highly skewed toward elevated values: the mean Lp[a] level was 0.61 mg/ml (SD 0.45) as compared to 0.18 mg/ml (SD 0.16) in a normal Caucasian population (P < 0.0001). Phenotypes for apo[a] were identified by SDS-agarose-gel electrophoresis, followed by immunoblotting and detection by chemiluminescence. Seventeen different isoforms (ranging from 440 to 920 kDa) were found among all the animals as compared to 19 (540 to 960 kDa) in a human population of equivalent number. However, the distribution of apo[a] phenotypes was distinct between these populations. Thus isoforms of low molecular mass occurred with greater frequency in chimpanzee as compared to humans. In both populations, a strong inverse correlation between Lp[a] levels and apo[a] isoform sizes was found in chimpanzees (r = -0.48; P < 0.01) and in man (r = -0.68; P < 0.0002).(ABSTRACT TRUNCATED AT 250 WORDS)
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