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Characterization of apoM in normal and genetically modified mice

Faber, Kirsten LU ; Axler, Olof LU ; Dahlbäck, Björn LU and Nielsen, L (2004) In Journal of Lipid Research 45(7). p.1272-1278
Abstract
A novel human apolipoprotein [apolipoprotein M (apoM)l was recently described and demonstrated to be a lipocalin. We have now examined apoM in wild-type mice and mice with genetically altered lipoprotein metabolism. Liver and kidney showed high mRNA expression, whereas spleen, heart, brain, and testis demonstrated low expression. ApoM gene expression was initiated on embryonic day 10. Western blot analysis of plasma suggested that mouse apoM, like its human counterpart, is secreted with a retained signal peptide, but unlike human apoM it is not glycosylated. Gel filtration of plasma showed apoM to be associated with HDL-sized particles in wild-type and apoA-I-deficient mice and with HDL and LDL-sized particles in LDL receptor-deficient... (More)
A novel human apolipoprotein [apolipoprotein M (apoM)l was recently described and demonstrated to be a lipocalin. We have now examined apoM in wild-type mice and mice with genetically altered lipoprotein metabolism. Liver and kidney showed high mRNA expression, whereas spleen, heart, brain, and testis demonstrated low expression. ApoM gene expression was initiated on embryonic day 10. Western blot analysis of plasma suggested that mouse apoM, like its human counterpart, is secreted with a retained signal peptide, but unlike human apoM it is not glycosylated. Gel filtration of plasma showed apoM to be associated with HDL-sized particles in wild-type and apoA-I-deficient mice and with HDL and LDL-sized particles in LDL receptor-deficient mice, whereas apoM was mainly found in VLDL-sized particles in high-fat, high-cholesterol-fed apoE-deficient mice. The plasma concentration of apoM was similar in wild-type, LDL receptor-deficient, and apoE-deficient mice but was reduced to 33% in apoA-I-deficient compared with wild-type mice (P = 0.007). These data suggest that apoM mainly associates with HDL in normal mice but also with the pathologically increased lipoprotein fraction in genetically modified mice. The substantially decreased apoM levels in apoA-I-deficient mice suggest a connection between apoM and apoA-I metabolism.-Faber, K., O. Axler, B. Dahlback, and L. B. Nielsen. Characterization of apoM in normal and genetically modified mice. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
density lipoprotein, low, high density lipoprotein, apolipoprotein A-I, apolipoprotein M, very low density lipoprotein
in
Journal of Lipid Research
volume
45
issue
7
pages
1272 - 1278
publisher
American Society for Biochemistry and Molecular Biology
external identifiers
  • wos:000222186400009
  • pmid:15102887
  • scopus:3042560032
ISSN
1539-7262
DOI
10.1194/jlr.M300451-JLR200
language
English
LU publication?
yes
id
589eaa60-ccd3-4565-a3fc-408672410566 (old id 273819)
date added to LUP
2007-10-22 15:39:06
date last changed
2017-11-19 03:39:33
@article{589eaa60-ccd3-4565-a3fc-408672410566,
  abstract     = {A novel human apolipoprotein [apolipoprotein M (apoM)l was recently described and demonstrated to be a lipocalin. We have now examined apoM in wild-type mice and mice with genetically altered lipoprotein metabolism. Liver and kidney showed high mRNA expression, whereas spleen, heart, brain, and testis demonstrated low expression. ApoM gene expression was initiated on embryonic day 10. Western blot analysis of plasma suggested that mouse apoM, like its human counterpart, is secreted with a retained signal peptide, but unlike human apoM it is not glycosylated. Gel filtration of plasma showed apoM to be associated with HDL-sized particles in wild-type and apoA-I-deficient mice and with HDL and LDL-sized particles in LDL receptor-deficient mice, whereas apoM was mainly found in VLDL-sized particles in high-fat, high-cholesterol-fed apoE-deficient mice. The plasma concentration of apoM was similar in wild-type, LDL receptor-deficient, and apoE-deficient mice but was reduced to 33% in apoA-I-deficient compared with wild-type mice (P = 0.007). These data suggest that apoM mainly associates with HDL in normal mice but also with the pathologically increased lipoprotein fraction in genetically modified mice. The substantially decreased apoM levels in apoA-I-deficient mice suggest a connection between apoM and apoA-I metabolism.-Faber, K., O. Axler, B. Dahlback, and L. B. Nielsen. Characterization of apoM in normal and genetically modified mice.},
  author       = {Faber, Kirsten and Axler, Olof and Dahlbäck, Björn and Nielsen, L},
  issn         = {1539-7262},
  keyword      = {density lipoprotein,low,high density lipoprotein,apolipoprotein A-I,apolipoprotein M,very low density lipoprotein},
  language     = {eng},
  number       = {7},
  pages        = {1272--1278},
  publisher    = {American Society for Biochemistry and Molecular Biology},
  series       = {Journal of Lipid Research},
  title        = {Characterization of apoM in normal and genetically modified mice},
  url          = {http://dx.doi.org/10.1194/jlr.M300451-JLR200},
  volume       = {45},
  year         = {2004},
}