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Palmitic acid suppresses apolipoprotein M gene expression via the pathway of PPARβ/δ in HepG2 cells.

Luo, Guanghua ; Shi, Yuanping ; Zhang, Jun ; Mu, Qinfeng ; Qin, Li ; Zheng, Lu ; Feng, Yuehua ; Berggren Söderlund, Maria LU ; Nilsson-Ehle, Peter LU and Zhang, Xiaoying , et al. (2014) In Biochemical and Biophysical Research Communications 445(1). p.203-207
Abstract
It has been demonstrated that apolipoprotein M (APOM) is a vasculoprotective constituent of high density lipoprotein (HDL), which could be related to the anti-atherosclerotic property of HDL. Investigation of regulation of APOM expression is of important for further exploring its pathophysiological function in vivo. Our previous studies indicated that expression of APOM could be regulated by platelet activating factor (PAF), transforming growth factors (TGF), insulin-like growth factor (IGF), leptin, hyperglycemia and etc., in vivo and/or in vitro. In the present study, we demonstrated that palmitic acid could significantly inhibit APOM gene expression in HepG2 cells. Further study indicated neither PI-3 kinase (PI3K) inhibitor LY294002... (More)
It has been demonstrated that apolipoprotein M (APOM) is a vasculoprotective constituent of high density lipoprotein (HDL), which could be related to the anti-atherosclerotic property of HDL. Investigation of regulation of APOM expression is of important for further exploring its pathophysiological function in vivo. Our previous studies indicated that expression of APOM could be regulated by platelet activating factor (PAF), transforming growth factors (TGF), insulin-like growth factor (IGF), leptin, hyperglycemia and etc., in vivo and/or in vitro. In the present study, we demonstrated that palmitic acid could significantly inhibit APOM gene expression in HepG2 cells. Further study indicated neither PI-3 kinase (PI3K) inhibitor LY294002 nor protein kinase C (PKC) inhibitor GFX could abolish palmitic acid induced down-regulation of APOM expression. In contrast, the peroxisome proliferator-activated receptor beta/delta (PPARβ/δ) antagonist GSK3787 could totally reverse the palmitic acid-induced down-regulation of APOM expression, which clearly demonstrates that down-regulation of APOM expression induced by palmitic acid is mediated via the PPARβ/δ pathway. (Less)
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organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Biochemical and Biophysical Research Communications
volume
445
issue
1
pages
203 - 207
publisher
Elsevier
external identifiers
  • pmid:24508264
  • wos:000332749400035
  • scopus:84896736470
  • pmid:24508264
ISSN
1090-2104
DOI
10.1016/j.bbrc.2014.01.170
language
English
LU publication?
yes
id
67dd5b9c-71a2-4c14-968c-6ee6868ab919 (old id 4335115)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/24508264?dopt=Abstract
date added to LUP
2016-04-01 10:11:03
date last changed
2022-04-04 03:14:19
@article{67dd5b9c-71a2-4c14-968c-6ee6868ab919,
  abstract     = {{It has been demonstrated that apolipoprotein M (APOM) is a vasculoprotective constituent of high density lipoprotein (HDL), which could be related to the anti-atherosclerotic property of HDL. Investigation of regulation of APOM expression is of important for further exploring its pathophysiological function in vivo. Our previous studies indicated that expression of APOM could be regulated by platelet activating factor (PAF), transforming growth factors (TGF), insulin-like growth factor (IGF), leptin, hyperglycemia and etc., in vivo and/or in vitro. In the present study, we demonstrated that palmitic acid could significantly inhibit APOM gene expression in HepG2 cells. Further study indicated neither PI-3 kinase (PI3K) inhibitor LY294002 nor protein kinase C (PKC) inhibitor GFX could abolish palmitic acid induced down-regulation of APOM expression. In contrast, the peroxisome proliferator-activated receptor beta/delta (PPARβ/δ) antagonist GSK3787 could totally reverse the palmitic acid-induced down-regulation of APOM expression, which clearly demonstrates that down-regulation of APOM expression induced by palmitic acid is mediated via the PPARβ/δ pathway.}},
  author       = {{Luo, Guanghua and Shi, Yuanping and Zhang, Jun and Mu, Qinfeng and Qin, Li and Zheng, Lu and Feng, Yuehua and Berggren Söderlund, Maria and Nilsson-Ehle, Peter and Zhang, Xiaoying and Xu, Ning}},
  issn         = {{1090-2104}},
  language     = {{eng}},
  number       = {{1}},
  pages        = {{203--207}},
  publisher    = {{Elsevier}},
  series       = {{Biochemical and Biophysical Research Communications}},
  title        = {{Palmitic acid suppresses apolipoprotein M gene expression via the pathway of PPARβ/δ in HepG2 cells.}},
  url          = {{https://lup.lub.lu.se/search/files/1633212/4611846.pdf}},
  doi          = {{10.1016/j.bbrc.2014.01.170}},
  volume       = {{445}},
  year         = {{2014}},
}