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Characterization of apoM in normal and genetically modified mice
Kirsten Faber1, Olof Axler, Björn Dahlbäck
1Division of Clinical Chemistry, Department of Laboratory Medicine, University of Lund, University Hospital Malmo, S-20502 Malmo, Sweden.
Journal of Lipid Research
|April 23, 2004
Summary
Apolipoprotein M (apoM) is a lipocalin found in mouse plasma, primarily associated with HDL. Its levels significantly decrease in apoA-I-deficient mice, suggesting a link to apoA-I metabolism.
Area of Science:
- Biochemistry
- Molecular Biology
- Genetics
Background:
- A novel human apolipoprotein, apolipoprotein M (apoM), a lipocalin, has been identified.
- Understanding apoM's role in lipoprotein metabolism requires further investigation in animal models.
Purpose of the Study:
- To characterize apolipoprotein M (apoM) expression and lipoprotein association in mice.
- To investigate the relationship between apoM and lipoprotein metabolism in genetically modified mouse models.
Main Methods:
- Examined apoM mRNA expression in various mouse tissues.
- Analyzed plasma apoM secretion and glycosylation using Western blot.
- Determined apoM association with lipoprotein particles (HDL, LDL, VLDL) via gel filtration.
- Measured plasma apoM concentrations in wild-type and genetically altered mice (apoA-I, LDL receptor, apoE deficient).
Main Results:
- High apoM mRNA expression observed in liver and kidney; low expression in spleen, heart, brain, and testis.
- Mouse apoM is secreted with a retained signal peptide but is not glycosylated, unlike human apoM.
- In wild-type and apoA-I-deficient mice, apoM associates with HDL-sized particles.
- In LDL receptor-deficient mice, apoM associates with HDL- and LDL-sized particles.
- In apoE-deficient mice, apoM is primarily found in VLDL-sized particles.
- Plasma apoM concentration is similar in wild-type, LDL receptor-deficient, and apoE-deficient mice.
- Plasma apoM levels are significantly reduced (33%) in apoA-I-deficient mice compared to wild-type.
Conclusions:
- Apolipoprotein M primarily associates with HDL in normal mice.
- In genetically modified mice with altered lipoprotein profiles, apoM associates with these pathological fractions.
- The substantial decrease in apoM levels in apoA-I-deficient mice indicates a significant connection between apoM and apoA-I metabolism.
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