Kynurenic acid attenuates pro-inflammatory reactions in lipopolysaccharide-stimulated endothelial cells through the PPARδ/HO-1-dependent pathway

Taeseung Lee, Hyung Sub Park, Ji Hoon Jeong, Tae Woo Jung

Research output: Contribution to journalArticleResearchpeer-review

Abstract

Kynurenic acid (KA) regulates energy homeostasis and alleviates inflammation in adipose tissue but how KA affects the atherosclerotic response in HUVECs remains unclear. We evaluated the effects of KA on lipopolysaccharide (LPS)-induced inflammation and apoptosis in HUVECs. KA enhanced peroxisome proliferator-activated receptor delta (PPARδ) expression in HUVECs and THP-1 cells and suppressed LPS-induced atherosclerotic responses through PPARδ-mediated signaling. Moreover, KA treatment mitigated LPS-induced phosphorylation of nuclear factor kappa B and pro-inflammatory cytokine release in HUVECs and THP-1 cells, and down-regulated adhesion molecules in HUVECs and adhesion of THP-1 cells to HUVECs following LPS treatment. KA treatment decreased LPS-induced inflammation and apoptosis, and also promoted heme oxygenase (HO)-1 expression, which suppresses inflammation in HUVECs. Suppression of PPARδ or HO-1 expression markedly mitigated the effects of KA on atherosclerotic responses in HUVECs. Thus, KA attenuates LPS-induced atherosclerotic responses by suppressing inflammation via the PPARδ/HO-1-dependent pathway.

Original languageEnglish
Article number110510
JournalMolecular and Cellular Endocrinology
Volume495
DOIs
StatePublished - 15 Sep 2019

Fingerprint

PPAR delta
Kynurenic Acid
Heme Oxygenase-1
Endothelial cells
Lipopolysaccharides
Endothelial Cells
Inflammation
Adhesion
Apoptosis
Phosphorylation
NF-kappa B
Human Umbilical Vein Endothelial Cells
Adipose Tissue
Homeostasis
Tissue
Cytokines
Molecules

Keywords

  • Atherosclerosis
  • Endothelium
  • HUVEC
  • Inflammation
  • Kynurenic acid
  • Obesity

Cite this

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title = "Kynurenic acid attenuates pro-inflammatory reactions in lipopolysaccharide-stimulated endothelial cells through the PPARδ/HO-1-dependent pathway",
abstract = "Kynurenic acid (KA) regulates energy homeostasis and alleviates inflammation in adipose tissue but how KA affects the atherosclerotic response in HUVECs remains unclear. We evaluated the effects of KA on lipopolysaccharide (LPS)-induced inflammation and apoptosis in HUVECs. KA enhanced peroxisome proliferator-activated receptor delta (PPARδ) expression in HUVECs and THP-1 cells and suppressed LPS-induced atherosclerotic responses through PPARδ-mediated signaling. Moreover, KA treatment mitigated LPS-induced phosphorylation of nuclear factor kappa B and pro-inflammatory cytokine release in HUVECs and THP-1 cells, and down-regulated adhesion molecules in HUVECs and adhesion of THP-1 cells to HUVECs following LPS treatment. KA treatment decreased LPS-induced inflammation and apoptosis, and also promoted heme oxygenase (HO)-1 expression, which suppresses inflammation in HUVECs. Suppression of PPARδ or HO-1 expression markedly mitigated the effects of KA on atherosclerotic responses in HUVECs. Thus, KA attenuates LPS-induced atherosclerotic responses by suppressing inflammation via the PPARδ/HO-1-dependent pathway.",
keywords = "Atherosclerosis, Endothelium, HUVEC, Inflammation, Kynurenic acid, Obesity",
author = "Taeseung Lee and Park, {Hyung Sub} and Jeong, {Ji Hoon} and Jung, {Tae Woo}",
year = "2019",
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Kynurenic acid attenuates pro-inflammatory reactions in lipopolysaccharide-stimulated endothelial cells through the PPARδ/HO-1-dependent pathway. / Lee, Taeseung; Park, Hyung Sub; Jeong, Ji Hoon; Jung, Tae Woo.

In: Molecular and Cellular Endocrinology, Vol. 495, 110510, 15.09.2019.

Research output: Contribution to journalArticleResearchpeer-review

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N2 - Kynurenic acid (KA) regulates energy homeostasis and alleviates inflammation in adipose tissue but how KA affects the atherosclerotic response in HUVECs remains unclear. We evaluated the effects of KA on lipopolysaccharide (LPS)-induced inflammation and apoptosis in HUVECs. KA enhanced peroxisome proliferator-activated receptor delta (PPARδ) expression in HUVECs and THP-1 cells and suppressed LPS-induced atherosclerotic responses through PPARδ-mediated signaling. Moreover, KA treatment mitigated LPS-induced phosphorylation of nuclear factor kappa B and pro-inflammatory cytokine release in HUVECs and THP-1 cells, and down-regulated adhesion molecules in HUVECs and adhesion of THP-1 cells to HUVECs following LPS treatment. KA treatment decreased LPS-induced inflammation and apoptosis, and also promoted heme oxygenase (HO)-1 expression, which suppresses inflammation in HUVECs. Suppression of PPARδ or HO-1 expression markedly mitigated the effects of KA on atherosclerotic responses in HUVECs. Thus, KA attenuates LPS-induced atherosclerotic responses by suppressing inflammation via the PPARδ/HO-1-dependent pathway.

AB - Kynurenic acid (KA) regulates energy homeostasis and alleviates inflammation in adipose tissue but how KA affects the atherosclerotic response in HUVECs remains unclear. We evaluated the effects of KA on lipopolysaccharide (LPS)-induced inflammation and apoptosis in HUVECs. KA enhanced peroxisome proliferator-activated receptor delta (PPARδ) expression in HUVECs and THP-1 cells and suppressed LPS-induced atherosclerotic responses through PPARδ-mediated signaling. Moreover, KA treatment mitigated LPS-induced phosphorylation of nuclear factor kappa B and pro-inflammatory cytokine release in HUVECs and THP-1 cells, and down-regulated adhesion molecules in HUVECs and adhesion of THP-1 cells to HUVECs following LPS treatment. KA treatment decreased LPS-induced inflammation and apoptosis, and also promoted heme oxygenase (HO)-1 expression, which suppresses inflammation in HUVECs. Suppression of PPARδ or HO-1 expression markedly mitigated the effects of KA on atherosclerotic responses in HUVECs. Thus, KA attenuates LPS-induced atherosclerotic responses by suppressing inflammation via the PPARδ/HO-1-dependent pathway.

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