Conjugated linoleic acid suppresses the migratory and inflammatory phenotype of the monocyte/macrophage cell

McClelland, Sarah E.; Cox, Clare; O'Connor, R.; Gaetano, Monica de; McCarthy, Cathal; Cryan, Lorna M.; Fitzgerald, Des; Belton, Orina

doi:10.1016/j.atherosclerosis.2010.02.003

Cited by 43 publications

(36 citation statements)

References 29 publications

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“…It was found that PUFA could inhibit palmitate-induced increase in expression of LOX1 and fatty acid-binding protein (FABP) [87]. Conjugated linoleic acid was shown to diminish atherosclerosis progression in mice through peroxisome proliferator-activated receptor γ (PPARγ)-dependent mechanism involving down-regulation of expression of proinflammatory genes such as NFκB, CCL2, MMP-9, phospholipase 2, and cyclooxygenase 2 specifically in macrophages [88].…”

Section: Effects Of Proinflammatory Lipid Modulators On Macrophage Phmentioning

confidence: 98%

RETRACTED: Macrophage phenotypic plasticity in atherosclerosis: The associated features and the peculiarities of the expression of inflammatory genes

Chistiakov

Bobryshev

Nikiforov

et al. 2015

International Journal of Cardiology

163

138

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Section: Effects Of Proinflammatory Lipid Modulators On Macrophage Phmentioning

confidence: 98%

RETRACTED: Macrophage phenotypic plasticity in atherosclerosis: The associated features and the peculiarities of the expression of inflammatory genes

Chistiakov

Bobryshev

Nikiforov

et al. 2015

International Journal of Cardiology

163

138

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“…Subcutaneous administration of nitro-oleate was recently shown to potently inhibit atheroma formation in ApoE-deficient mice (1518). It is tempting to speculate that the surprising anti-atherosclerotic effects of so-called "conjugated linoleic acid" might be mediated by similar mechanisms (1166). 15d-PGJ 2 can covalently bind and activate the strongly anti-inflammatory PPAR␥.…”

Section: F Modulation Of Signaling By Electrophilesmentioning

confidence: 99%

Molecular Biology of Atherosclerosis

Hopkins

2013

Physiological Reviews

389

344

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At least 468 individual genes have been manipulated by molecular methods to study their effects on the initiation, promotion, and progression of atherosclerosis. Most clinicians and many investigators, even in related disciplines, find many of these genes and the related pathways entirely foreign. Medical schools generally do not attempt to incorporate the relevant molecular biology into their curriculum. A number of key signaling pathways are highly relevant to atherogenesis and are presented to provide a context for the gene manipulations summarized herein. The pathways include the following: the insulin receptor (and other receptor tyrosine kinases); Ras and MAPK activation; TNF-␣ and related family members leading to activation of NF-B; effects of reactive oxygen species (ROS) on signaling; endothelial adaptations to flow including G protein-coupled receptor (GPCR) and integrin-related signaling; activation of endothelial and other cells by modified lipoproteins; purinergic signaling; control of leukocyte adhesion to endothelium, migration, and further activation; foam cell formation; and macrophage and vascular smooth muscle cell signaling related to proliferation, efferocytosis, and apoptosis. This review is intended primarily as an introduction to these key signaling pathways. They have become the focus of modern atherosclerosis research and will undoubtedly provide a rich resource for future innovation toward intervention and prevention of the number one cause of death in the modern world.

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“…fat depots (Akter et al, 2011). Moreover, CLA can influence MCP-1 expression in human adipocytes; however, either inducing (Martinez et al, 2013) or inhibiting (McClelland et al, 2010) effects of CLA on MCP-1 in human adipocytes are reported.…”

Section: Short Communicationmentioning

confidence: 85%

Short communication: Localization and expression of monocyte chemoattractant protein-1 in different subcutaneous and visceral adipose tissues of early-lactating dairy cows

Häußler

Sacré

Friedauer

et al. 2015

Journal of Dairy Science

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The present study aimed to examine the mRNA abundance of the monocyte chemoattractant protein-1 (MCP-1) and to localize the MCP-1 protein in different subcutaneous (s.c.) and visceral (v.c.) fat depots in high-yielding dairy cows. Early-lactating German Holstein cows (n=25) were divided into a control (CON) and a conjugated linoleic acids (CLA)-supplemented group to investigate potential effects of dietary CLA treatment on MCP-1. The MCP-1 was localized in different s.c. and v.c. adipose tissue (AT) by immunohistochemistry, whereas the mRNA abundance was investigated using quantitative PCR. Albeit the infiltration of immune cells into bovine AT has been demonstrated to be only marginal, both MCP-1 protein and mRNA could be detected in bovine AT depots. The MCP-1 protein was localized both in the cytoplasm of adipocytes and in the cytoplasm of cells from the stromal vascular fraction; however, the number of MCP-1-positive cells was low. The mRNA abundances of MCP-1 were higher in v.c. compared with s.c. AT. Moreover, neither mRNA abundance nor protein expression of MCP-1 was seriously influenced by CLA supplementation of early-lactating dairy cows.

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Conjugated linoleic acid suppresses the migratory and inflammatory phenotype of the monocyte/macrophage cell

Cited by 43 publications

References 29 publications

RETRACTED: Macrophage phenotypic plasticity in atherosclerosis: The associated features and the peculiarities of the expression of inflammatory genes

RETRACTED: Macrophage phenotypic plasticity in atherosclerosis: The associated features and the peculiarities of the expression of inflammatory genes

Molecular Biology of Atherosclerosis

Short communication: Localization and expression of monocyte chemoattractant protein-1 in different subcutaneous and visceral adipose tissues of early-lactating dairy cows

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