Differential apolipoprotein(a) isoform expression in heterozygosity is an independent contributor to lipoprotein(a) levels variability

Background and methods: Lipoprotein(a) [Lp(a)] levels represent an independent risk factor for cardio- and cerebrovascular diseases. Since lipoprotein(a) levels show a wide variability even in subjects with similar apolipoprotein(a) isoforms, we investigated the contribution of apolipoprotein(a) het...

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Bibliographic Details
Published in:Clinica chimica acta 2003-02, Vol.328 (1), p.91-97
Main Authors: Noto, Davide, Pace, Antonio, Cefalù, Angelo B., Barbagallo, Carlo M., Rizzo, Manfredi, Marino, Giuseppina, Emmanuele, Giovanni, Travali, Salvatore, Notarbartolo, Alberto, Averna, Maurizio
Format: Article
Language:English
Subjects:
Adult
Aged
Apolipoprotein(a) phenotyping
Apolipoproteins - genetics
Apoprotein(a)
Biological and medical sciences
Female
Heterozygote
Humans
Investigative techniques, diagnostic techniques (general aspects)
Lipoprotein(a)
Lipoprotein(a) - blood
Lipoprotein(a) - genetics
Male
Medical sciences
Middle Aged
Miscellaneous. Technology
Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques
Protein expression
Protein Isoforms
Western blot
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Summary:Background and methods: Lipoprotein(a) [Lp(a)] levels represent an independent risk factor for cardio- and cerebrovascular diseases. Since lipoprotein(a) levels show a wide variability even in subjects with similar apolipoprotein(a) isoforms, we investigated the contribution of apolipoprotein(a) heterozygosity to lipoprotein(a) variance. Lipoprotein(a) levels, apolipoprotein(a) isoforms identification and expression, and the correlation with other lipo-apolipoprotein parameters have been investigated in 628 subjects >18 years of age. Results: In our study, 246 subjects were found heterozygous for apolipoprotein(a) isoforms. Lipoprotein(a) levels were higher in females. About 40% of the subjects expressed the larger isoform more intensely than the dominant isoform. Lipoprotein(a) was correlated with apolipoprotein(a) dominant isoform size, HDL-cholesterol and smaller apolipoprotein(a) isoform expression rate. Lipoprotein(a) was independently correlated with the smaller apolipoprotein(a) isoform, with its expression rate and with LDL-cholesterol. The inclusion of the smaller apolipoprotein(a) expression rate in a multiple regression model explained at least an additional 4% of the lipoprotein(a) variance after correction for apolipoprotein(a) size. Conclusions: The smaller isoforms are not always effectively dominant in heterozygosis since 40% of the subjects expressed more the larger isoform. The individual variability of apolipoprotein(a) isoform expression in heterozygosis could explain part of the lipoprotein(a) levels variability.
ISSN:0009-8981
1873-3492
DOI:10.1016/S0009-8981(02)00390-X