Inflammatory response of human coronary artery endothelial cells to saturated long-chain fatty acids

Krogmann, Alexander; Staiger, K.; Haas, Carina; Gommer, Nadja; Heni, Martin; Machicao, Fausto; Häring, Hans‐Ulrich; Staiger, Harald

doi:10.1016/j.mvr.2010.11.008

Cited by 39 publications

(27 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The endothelial cells can express 59 inflammatory genes, including chemokines, cytokines, chemokine and cytokine receptors, and inflammatory transcription factors, and thus, inflammatory cytokines will be consequently secreted by the inflammatory activation of endothelial cells [34]. As small and active proteins, cytokines regulate cellular growth, function, and differentiation as well as control the immune response and inflammation, including some proinflammatory cytokines such as IL-6 and IL-8 [35].…”

Section: Discussionmentioning

confidence: 99%

Effects of MicroRNA-499 On the Inflammatory Damage of Endothelial Cells During Coronary Artery Disease Via the Targeting of PDCD4 Through the NF-Κβ/TNF-α Signaling Pathway

Zhang¹,

He²,

Shi³

2017

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: This study aimed to analyze the impact of microRNA-499 (miR-499) on the inflammatory damage of endothelial cells during coronary artery disease (CAD) via the targeting of PDCD4 through the NF-kB/ TNF-α signaling pathway. Methods: A total of 216 CAD patients (CAD group) and 90 healthy people (normal group) were enrolled in our study. Endothelial cells were collected and assigned into normal, OX-LDL, negative control (NC), miR-499 inhibitor, miR-499 mimic, PDCD4 siRNA, and miR-499 inhibitor + PDCD4 siRNA groups. The qRT-PCR and western blotting were performed to detect the mRNA and protein expression levels of PDCD4 and miR-499. The MTT assay was performed to determine cell viability, ELISA was performed to determine the expression levels of inflammatory factors, and flow cytometry assay to evaluate cell apoptosis. Results: Increased miR-499 expression and decreased PDCD4 expression in the plasma were observed in the CAD group compared with the normal group, demonstrating a negative correlation between miR-499 and PDCD4. Compared to the normal and miR-499 inhibitor groups, the survival rate of cells and PDCD4 expression were decreased; and the expressions of miR-499, IL-6, IL-8, IL-1β, TNF-α, NF-kB, VCAM-1, ICAM-1 and MCP-1 and the apoptosis rate were all elevated in the OX-LDL, NC, miR-499 mimic, PDCD4 siRNA and miR-499 inhibitor + PDCD4 siRNA groups. Compared to the OX-LDL, NC and miR-499 inhibitor + PDCD4 siRNA groups, PDCD4 expression and the survival rate of cells were increased; and the IL-6, IL-8, IL-1β, TNF-α, NF-κB, VCAM-1, ICAM-1 and MCP-1 expression levels and the apoptosis rate were all reduced in the miR-499 inhibitor group. In the PDCD4 siRNA group, PDCD4 expression and the survival rate of cells were lower, and the expression levels of IL-6, IL-8, IL-1β, TNF-α, NF-κB, VCAM-1, ICAM-1 and MCP-1 and the apoptosis rate were all higher compared with the miR-499 mimic group. In the miR-499 inhibitor + PDCD4 siRNA group, PDCD4 expression and the survival rate of cells were higher, and the expression levels of IL-6, IL-8, IL-1β, TNF-α, NF-κB, VCAM-1, ICAM-1, and MCP-1 and the apoptosis rate were all lower than those in the PDCD4 siRNA group. Conclusion: Down-regulated miR-499 expression increased PDCD4 expression and protected endothelial cells from inflammatory damage during CAD by inhibiting the NF-κB/TNF-α signaling pathway.

show abstract

Section: Discussionmentioning

confidence: 99%

Effects of MicroRNA-499 On the Inflammatory Damage of Endothelial Cells During Coronary Artery Disease Via the Targeting of PDCD4 Through the NF-Κβ/TNF-α Signaling Pathway

Zhang¹,

He²,

Shi³

2017

Cell Physiol Biochem

View full text Add to dashboard Cite

show abstract

“…An important implication of these findings is that palmitate through interleukin-8 production may have a role in the recruitment of neutrophil and, consequently, in the establishment of an inflammatory state in this organ. Saturated fatty acids have been shown to activate inflammatory pathways in different cell types including skeletal muscle cells(Coll et al, 2008;Lambertucci et al, 2012), endothelial cells(Krogmann et al, 2011) and macrophages. Regarding ͳ͵ these latter cells, activation of toll like receptors including toll like receptor-2 and toll like receptor-4 and, more recently, the triggering of the NLRP3 inflammasome, have been demonstrated and the pathways downstream to them were implicated in the proinflammatory activation of these cells by LCSFAs(Anderson et al, 2012;Huang et al, 2012;Valdearcos et al, 2012;Vandanmagsar et al, 2011).…”

mentioning

confidence: 99%

Fatty acids as modulators of neutrophil recruitment, function and survival

Rodrigues

Sato

Curi

et al. 2016

European Journal of Pharmacology

View full text Add to dashboard Cite

“…Previous in vitro studies have shown that palmitate impairs the insulin-dependent activation of endothelial nitric oxide synthase (eNOS) via the phosphorylation of IRS-1, as well as inducing the expression of IL-6 and intercellular adhesion molecule 1 (ICAM1) and promoting apoptosis in ECs 70,71) . Palmitate also stimulates the expression of IL-8, CXCL3 and CCL20 in ECs in a manner dependent upon NF-κB signaling 72) . In addition, it has been reported that palmitate increases the levels of ROS in cultured ECs and smooth muscle cells (SMCs) 73,74) , activates the ER stress pathway in ECs 72) and alters the production of the extracellular matrix in cultured SMCs 75) .…”

Section: Vascular Lipotoxicity and Tlr4 Signalingmentioning

confidence: 99%

“…Palmitate also stimulates the expression of IL-8, CXCL3 and CCL20 in ECs in a manner dependent upon NF-κB signaling 72) . In addition, it has been reported that palmitate increases the levels of ROS in cultured ECs and smooth muscle cells (SMCs) 73,74) , activates the ER stress pathway in ECs 72) and alters the production of the extracellular matrix in cultured SMCs 75) . In vivo, an HFD activates NF-κB signaling in the aorta of wild-type mice but not Tlr4 −/− mice, while palmitate activates NF-κB signaling in aortic explants in a TLR4-dependent manner 26) .…”

Section: Vascular Lipotoxicity and Tlr4 Signalingmentioning

confidence: 99%

Toll-Like Receptor, Lipotoxicity and Chronic inflammation: The Pathological Link Between Obesity and Cardiometabolic Disease

Eguchi

Manabe

2014

JAT

View full text Add to dashboard Cite

The epidemic growth in the prevalence of obesity has made the impact of metabolic syndrome on cardiovascular events increasingly significant. Elevated visceral adiposity, the indispensable component of metabolic syndrome, is thought to play a primary role in the increasing incidence of cardiometabolic disorders. Importantly, obesity is not merely the simple expansion of adipose tissue mass; it also involves the activation of inflammatory processes within visceral adipose tissue. Adipose tissue inflammation on the one hand enhances the production of proinflammatory adipokines and on the other hand increases the release of free fatty acids via the activation of lipolysis. The adipokines and free fatty acids secreted from visceral fat then contribute to a cardiometabolic pathology. We herein summarize recent advances in our understanding of the mechanisms by which visceral obesity leads to the activation of inflammation in cardiovascular and metabolic tissues and promotes cardiometabolic disease. Our focus is on Toll-like receptor 4 signaling and free fatty acids as mediators of chronic inflammation in patients with metabolic syndrome and atherosclerosis.

show abstract

Inflammatory response of human coronary artery endothelial cells to saturated long-chain fatty acids

Cited by 39 publications

References 36 publications

Effects of MicroRNA-499 On the Inflammatory Damage of Endothelial Cells During Coronary Artery Disease Via the Targeting of PDCD4 Through the NF-Κβ/TNF-α Signaling Pathway

Effects of MicroRNA-499 On the Inflammatory Damage of Endothelial Cells During Coronary Artery Disease Via the Targeting of PDCD4 Through the NF-Κβ/TNF-α Signaling Pathway

Fatty acids as modulators of neutrophil recruitment, function and survival

Toll-Like Receptor, Lipotoxicity and Chronic inflammation: The Pathological Link Between Obesity and Cardiometabolic Disease

Contact Info

Product

Resources

About