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

Forskningsoutput: TidskriftsbidragArtikel i vetenskaplig tidskrift

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.

Detaljer

Författare
  • Guanghua Luo
  • Yuanping Shi
  • Jun Zhang
  • Qinfeng Mu
  • Li Qin
  • Lu Zheng
  • Yuehua Feng
  • Maria Berggren Söderlund
  • Peter Nilsson-Ehle
  • Xiaoying Zhang
  • Ning Xu
Enheter & grupper
Forskningsområden

Ämnesklassifikation (UKÄ) – OBLIGATORISK

  • Biologiska vetenskaper
Originalspråkengelska
Sidor (från-till)203-207
TidskriftBiochemical and Biophysical Research Communications
Volym445
Utgivningsnummer1
StatusPublished - 2014
PublikationskategoriForskning
Peer review utfördJa

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