Down-regulation of apolipoprotein M expression is mediated by phosphatidylinositol 3-kinase in HepG2 cells.
(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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/154552
- author
- Xu, Ning LU ; Ahrén, Bo LU ; Jiang, Jingting and Nilsson-Ehle, Peter LU
- organization
- publishing date
- 2006
- 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
- 2024-01-11 09:16:52
@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}},
keywords = {{line; insulin; PPARs; apolipoprotein M; phosphatidylinositol 3-kinase and HepG2 cell}},
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/files/4692600/625370.pdf}},
doi = {{10.1016/j.bbalip.2006.02.002}},
volume = {{1761}},
year = {{2006}},
}