Inhibition of macrophage adhesion activity by 9trans,11trans-conjugated linoleic acid

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

Conjugated linoleic acids (CLAs) have anti-atherogenic effects in both in vitro and animal models. Most studies on CLAs were performed with either a CLA mixture or purified 9. cis (Z),11. trans (E)-CLA or 10. E,12. Z-CLA isomers. However, the 9. E,11. E isomer has superior anti-carcinogenic and anti-inflammatory effects compared with the more abundant CLAs. The 9. E,11. E-CLA isomer specifically increases interleukin-1 receptor antagonist (IL-1Ra), an important anti-inflammatory mediator that is associated with decreased risk of coronary heart disease. The purpose of this present study was to determine if 9. E,11. E-CLA affects markers of atherogenesis via regulation of IL-1Ra. In human umbilical vein endothelial cells (HUVECs), 9. E,11. E-CLA decreased such atherogenesis-related genes as intercellular adhesion molecule-1, vascular cell adhesion molecule-1, monocyte chemoattractant protein-1, E-selectin, P-selectin and C-C motif chemokine receptor-2. Treatment of RAW 264.7 cells with 9. E,11. E-CLA decreased their adhesion to HUVECs. This effect was reversed by inhibiting the phosphoinositide 3-kinase or mouse target of rapamycin pathways. IL-1Ra-deficient RAW 264.7 cells (siIL-1Ra RAW) bind more efficiently to HUVECs compared with the control stable cells (si-control RAW). In addition, HUVECs treated with siIL-1Ra RAW-conditioned media induce significantly higher levels of intercellular adhesion molecule-1, vascular cell adhesion molecule-1, monocyte chemoattractant protein-1 and E-selectin than HUVECs treated with si-control RAW-conditioned media. Taken together, the data show that 9. E,11. E-CLA decreases the atherogenesis-related genes in HUVECs and alters adhesion of macrophages. In addition, the induction of IL-1Ra by 9. E,11. E-CLA is partially responsible for the anti-atherogenic properties of this particular CLA isomer.

Original languageEnglish (US)
Pages (from-to)490-497
Number of pages8
JournalJournal of Nutritional Biochemistry
Volume21
Issue number6
DOIs
StatePublished - Jun 1 2010

Fingerprint

Conjugated Linoleic Acids
Macrophages
Adhesion
Endothelial cells
Human Umbilical Vein Endothelial Cells
Interleukin-1 Receptors
Isomers
Atherosclerosis
E-Selectin
Vascular Cell Adhesion Molecule-1
Chemokine CCL2
Intercellular Adhesion Molecule-1
Conditioned Culture Medium
CCR Receptors
Anti-Inflammatory Agents
Genes
P-Selectin
1-Phosphatidylinositol 4-Kinase
Sirolimus
Phosphatidylinositols

All Science Journal Classification (ASJC) codes

  • Endocrinology, Diabetes and Metabolism
  • Biochemistry
  • Molecular Biology
  • Nutrition and Dietetics
  • Clinical Biochemistry

Cite this

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title = "Inhibition of macrophage adhesion activity by 9trans,11trans-conjugated linoleic acid",
abstract = "Conjugated linoleic acids (CLAs) have anti-atherogenic effects in both in vitro and animal models. Most studies on CLAs were performed with either a CLA mixture or purified 9. cis (Z),11. trans (E)-CLA or 10. E,12. Z-CLA isomers. However, the 9. E,11. E isomer has superior anti-carcinogenic and anti-inflammatory effects compared with the more abundant CLAs. The 9. E,11. E-CLA isomer specifically increases interleukin-1 receptor antagonist (IL-1Ra), an important anti-inflammatory mediator that is associated with decreased risk of coronary heart disease. The purpose of this present study was to determine if 9. E,11. E-CLA affects markers of atherogenesis via regulation of IL-1Ra. In human umbilical vein endothelial cells (HUVECs), 9. E,11. E-CLA decreased such atherogenesis-related genes as intercellular adhesion molecule-1, vascular cell adhesion molecule-1, monocyte chemoattractant protein-1, E-selectin, P-selectin and C-C motif chemokine receptor-2. Treatment of RAW 264.7 cells with 9. E,11. E-CLA decreased their adhesion to HUVECs. This effect was reversed by inhibiting the phosphoinositide 3-kinase or mouse target of rapamycin pathways. IL-1Ra-deficient RAW 264.7 cells (siIL-1Ra RAW) bind more efficiently to HUVECs compared with the control stable cells (si-control RAW). In addition, HUVECs treated with siIL-1Ra RAW-conditioned media induce significantly higher levels of intercellular adhesion molecule-1, vascular cell adhesion molecule-1, monocyte chemoattractant protein-1 and E-selectin than HUVECs treated with si-control RAW-conditioned media. Taken together, the data show that 9. E,11. E-CLA decreases the atherogenesis-related genes in HUVECs and alters adhesion of macrophages. In addition, the induction of IL-1Ra by 9. E,11. E-CLA is partially responsible for the anti-atherogenic properties of this particular CLA isomer.",
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Inhibition of macrophage adhesion activity by 9trans,11trans-conjugated linoleic acid. / Lee, Yunkyoung; Vanden Heuvel, John Patrick.

In: Journal of Nutritional Biochemistry, Vol. 21, No. 6, 01.06.2010, p. 490-497.

Research output: Contribution to journalArticle

TY - JOUR

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AU - Lee, Yunkyoung

AU - Vanden Heuvel, John Patrick

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N2 - Conjugated linoleic acids (CLAs) have anti-atherogenic effects in both in vitro and animal models. Most studies on CLAs were performed with either a CLA mixture or purified 9. cis (Z),11. trans (E)-CLA or 10. E,12. Z-CLA isomers. However, the 9. E,11. E isomer has superior anti-carcinogenic and anti-inflammatory effects compared with the more abundant CLAs. The 9. E,11. E-CLA isomer specifically increases interleukin-1 receptor antagonist (IL-1Ra), an important anti-inflammatory mediator that is associated with decreased risk of coronary heart disease. The purpose of this present study was to determine if 9. E,11. E-CLA affects markers of atherogenesis via regulation of IL-1Ra. In human umbilical vein endothelial cells (HUVECs), 9. E,11. E-CLA decreased such atherogenesis-related genes as intercellular adhesion molecule-1, vascular cell adhesion molecule-1, monocyte chemoattractant protein-1, E-selectin, P-selectin and C-C motif chemokine receptor-2. Treatment of RAW 264.7 cells with 9. E,11. E-CLA decreased their adhesion to HUVECs. This effect was reversed by inhibiting the phosphoinositide 3-kinase or mouse target of rapamycin pathways. IL-1Ra-deficient RAW 264.7 cells (siIL-1Ra RAW) bind more efficiently to HUVECs compared with the control stable cells (si-control RAW). In addition, HUVECs treated with siIL-1Ra RAW-conditioned media induce significantly higher levels of intercellular adhesion molecule-1, vascular cell adhesion molecule-1, monocyte chemoattractant protein-1 and E-selectin than HUVECs treated with si-control RAW-conditioned media. Taken together, the data show that 9. E,11. E-CLA decreases the atherogenesis-related genes in HUVECs and alters adhesion of macrophages. In addition, the induction of IL-1Ra by 9. E,11. E-CLA is partially responsible for the anti-atherogenic properties of this particular CLA isomer.

AB - Conjugated linoleic acids (CLAs) have anti-atherogenic effects in both in vitro and animal models. Most studies on CLAs were performed with either a CLA mixture or purified 9. cis (Z),11. trans (E)-CLA or 10. E,12. Z-CLA isomers. However, the 9. E,11. E isomer has superior anti-carcinogenic and anti-inflammatory effects compared with the more abundant CLAs. The 9. E,11. E-CLA isomer specifically increases interleukin-1 receptor antagonist (IL-1Ra), an important anti-inflammatory mediator that is associated with decreased risk of coronary heart disease. The purpose of this present study was to determine if 9. E,11. E-CLA affects markers of atherogenesis via regulation of IL-1Ra. In human umbilical vein endothelial cells (HUVECs), 9. E,11. E-CLA decreased such atherogenesis-related genes as intercellular adhesion molecule-1, vascular cell adhesion molecule-1, monocyte chemoattractant protein-1, E-selectin, P-selectin and C-C motif chemokine receptor-2. Treatment of RAW 264.7 cells with 9. E,11. E-CLA decreased their adhesion to HUVECs. This effect was reversed by inhibiting the phosphoinositide 3-kinase or mouse target of rapamycin pathways. IL-1Ra-deficient RAW 264.7 cells (siIL-1Ra RAW) bind more efficiently to HUVECs compared with the control stable cells (si-control RAW). In addition, HUVECs treated with siIL-1Ra RAW-conditioned media induce significantly higher levels of intercellular adhesion molecule-1, vascular cell adhesion molecule-1, monocyte chemoattractant protein-1 and E-selectin than HUVECs treated with si-control RAW-conditioned media. Taken together, the data show that 9. E,11. E-CLA decreases the atherogenesis-related genes in HUVECs and alters adhesion of macrophages. In addition, the induction of IL-1Ra by 9. E,11. E-CLA is partially responsible for the anti-atherogenic properties of this particular CLA isomer.

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