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Down-regulation of apolipoprotein M expression is mediated by phosphatidylinositol 3-kinase in HepG2 cells.

Xu, Ning LU ; Ahrén, Bo LU ; Jiang, Jingting and Nilsson-Ehle, Peter LU (2006) In Biochimica et Biophysica Acta - Molecular and Cell Biology of Lipids 1761(2). p.256-260
Abstract
Apolipoprotein M (apoM) is a novel apolipoprotein present mostly in high-density lipoprotein (HDL) in human plasma. In the present study, we demonstrate that insulin, insulin-like growth factor I (IGF-I), and IGF-I potential peptide (IGF-IPP) significantly inhibits apoM expression, in a dose- and a time-dependent manner, in the human hepatoma cell line, HepG2 cells. Insulin-induced down-regulation of apoM was blocked by AG1024 (a specific insulin receptor inhibitor) and LY294002 (a phosphatidylinositol 3-kinase (PI3K) inhibitor), which indicates that it is mediated via the activation of PI3K pathway. In contrast, PD98059 (a MAP kinase inhibitor) did not influence insulin-induced down-regulation of apoM expression, and activation of neither... (More)
Apolipoprotein M (apoM) is a novel apolipoprotein present mostly in high-density lipoprotein (HDL) in human plasma. In the present study, we demonstrate that insulin, insulin-like growth factor I (IGF-I), and IGF-I potential peptide (IGF-IPP) significantly inhibits apoM expression, in a dose- and a time-dependent manner, in the human hepatoma cell line, HepG2 cells. Insulin-induced down-regulation of apoM was blocked by AG1024 (a specific insulin receptor inhibitor) and LY294002 (a phosphatidylinositol 3-kinase (PI3K) inhibitor), which indicates that it is mediated via the activation of PI3K pathway. In contrast, PD98059 (a MAP kinase inhibitor) did not influence insulin-induced down-regulation of apoM expression, and activation of neither PPAR-alpha agonist (GW7647) nor PPAR-gamma agonist (GW1929) influences apoM expression in HepG2 cells, which indicates that regulation of apoM expression is not related to the activation of PPAR-alpha and PPAR-gamma in hepatic cells, whereas, both PPAR-Of and PPAR-gamma agonists could inhibit apoB expression. Moreover, in the present study, we demonstrated that PPAR beta/delta agonist (GW501516) could inhibit both apoM and apoB expression in the HepG2 cells. In conclusion, this study shows that apoM expression is regulated by PI3-kinase in HepG2-cells. (c) 2006 Elsevier B.V. All rights reserved. (Less)
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author
; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
line, insulin, PPARs, apolipoprotein M, phosphatidylinositol 3-kinase and HepG2 cell
in
Biochimica et Biophysica Acta - Molecular and Cell Biology of Lipids
volume
1761
issue
2
pages
256 - 260
publisher
Elsevier
external identifiers
  • pmid:16542871
  • wos:000236929500014
  • scopus:33646198232
ISSN
1388-1981
DOI
10.1016/j.bbalip.2006.02.002
language
English
LU publication?
yes
id
84e13611-162e-4bc4-b2d0-4cf60e4259b9 (old id 154552)
alternative location
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=16542871&dopt=Abstract
date added to LUP
2016-04-01 16:30:14
date last changed
2020-09-09 03:34:16
@article{84e13611-162e-4bc4-b2d0-4cf60e4259b9,
  abstract     = {Apolipoprotein M (apoM) is a novel apolipoprotein present mostly in high-density lipoprotein (HDL) in human plasma. In the present study, we demonstrate that insulin, insulin-like growth factor I (IGF-I), and IGF-I potential peptide (IGF-IPP) significantly inhibits apoM expression, in a dose- and a time-dependent manner, in the human hepatoma cell line, HepG2 cells. Insulin-induced down-regulation of apoM was blocked by AG1024 (a specific insulin receptor inhibitor) and LY294002 (a phosphatidylinositol 3-kinase (PI3K) inhibitor), which indicates that it is mediated via the activation of PI3K pathway. In contrast, PD98059 (a MAP kinase inhibitor) did not influence insulin-induced down-regulation of apoM expression, and activation of neither PPAR-alpha agonist (GW7647) nor PPAR-gamma agonist (GW1929) influences apoM expression in HepG2 cells, which indicates that regulation of apoM expression is not related to the activation of PPAR-alpha and PPAR-gamma in hepatic cells, whereas, both PPAR-Of and PPAR-gamma agonists could inhibit apoB expression. Moreover, in the present study, we demonstrated that PPAR beta/delta agonist (GW501516) could inhibit both apoM and apoB expression in the HepG2 cells. In conclusion, this study shows that apoM expression is regulated by PI3-kinase in HepG2-cells. (c) 2006 Elsevier B.V. All rights reserved.},
  author       = {Xu, Ning and Ahrén, Bo and Jiang, Jingting and Nilsson-Ehle, Peter},
  issn         = {1388-1981},
  language     = {eng},
  number       = {2},
  pages        = {256--260},
  publisher    = {Elsevier},
  series       = {Biochimica et Biophysica Acta - Molecular and Cell Biology of Lipids},
  title        = {Down-regulation of apolipoprotein M expression is mediated by phosphatidylinositol 3-kinase in HepG2 cells.},
  url          = {https://lup.lub.lu.se/search/ws/files/4692600/625370.pdf},
  doi          = {10.1016/j.bbalip.2006.02.002},
  volume       = {1761},
  year         = {2006},
}