Saturated, but Not Unsaturated, Fatty Acids Induce Apoptosis of Human Coronary Artery Endothelial Cells via Nuclear Factor- B Activation

Diabetes ◽  
2006 ◽  
Vol 55 (11) ◽  
pp. 3121-3126 ◽  
Author(s):  
K. Staiger ◽  
H. Staiger ◽  
C. Weigert ◽  
C. Haas ◽  
H.-U. Haring ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Endothelial Cells ◽  
Coronary Artery ◽  
Unsaturated Fatty Acids ◽  
Nuclear Factor ◽  
Human Coronary Artery ◽  
Factor B

scholarly journals p38 Mitogen-Activated Protein Kinase Mediates Palmitate-Induced Apoptosis But Not Inhibitor of Nuclear Factor-κB Degradation in Human Coronary Artery Endothelial Cells

Endocrinology ◽  
2007 ◽  
Vol 148 (4) ◽  
pp. 1622-1628 ◽  
Author(s):  
Weidong Chai ◽  
Zhenqi Liu
Keyword(s):  
Fatty Acids ◽  
Endothelial Cells ◽  
Coronary Artery ◽  
P38 Mapk ◽  
Fold Increase ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Human Coronary Artery ◽  
Mapk Activity ◽  
Induced Apoptosis

Plasma free fatty acids are elevated in patients with type 2 diabetes and contribute to the pathogenesis of insulin resistance and endothelial dysfunction. The p38 MAPK mediates stress, inflammation, and apoptosis. Whether free fatty acids induce apoptosis and/or activate nuclear factor-κB inflammatory pathway in human coronary artery endothelial cells (hCAECs) and, if so, whether this involves the p38 MAPK pathway is unknown. hCAECs (passages 4–6) were grown to 70% confluence and then incubated with palmitate at concentrations of 0–300 μm for 6–48 h. Palmitate at 100, 200, or 300 μm markedly increased apoptosis after 12 h of incubation. This apoptotic effect was time (P = 0.008) and dose (P = 0.006) dependent. Palmitate (100 μm for 24 h) induced a greater than 2-fold increase in apoptosis, which was accompanied with a 4-fold increase in p38 MAPK activity (P < 0.001). Palmitate did not affect the phosphorylation of Akt1 or ERK1/2. SB203580 (a specific inhibitor of p38 MAPK) alone did not affect cellular apoptosis; however, it abolished palmitate-induced apoptosis and p38 MAPK activation. Palmitate significantly reduced the level of inhibitor of nuclear factor-κB (IκB). However, treatment of cells with SB203580 did not restore IκB to baseline. We conclude that palmitate induces hCAEC apoptosis via a p38 MAPK-dependent mechanism and may participate in coronary endothelial injury in diabetes. However, palmitate-mediated IκB degradation in hCAECs is independent of p38 MAPK activity.

Ficus deltoidea reduces expression of interleukin 6 via nuclear factor kappa b pathway in human coronary artery endothelial cells

2017 ◽  
Vol 263 ◽  
pp. e122
Author(s):  
Suhaila Muid ◽  
Effat Omar ◽  
Radzi Ikhsan Ahmad ◽  
Nor Hadiani Ismail ◽  
Noor Alicezah Mohd Kasim ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Coronary Artery ◽  
Interleukin 6 ◽  
Nuclear Factor Kappa B ◽  
Nuclear Factor ◽  
Human Coronary Artery ◽  
Ficus Deltoidea ◽  
Nuclear Factor Kappa

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

2011 ◽  
Vol 81 (1) ◽  
pp. 52-59 ◽  
Author(s):  
Alexander Krogmann ◽  
Katrin Staiger ◽  
Carina Haas ◽  
Nadja Gommer ◽  
Andreas Peter ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Endothelial Cells ◽  
Coronary Artery ◽  
Inflammatory Response ◽  
Long Chain Fatty Acids ◽  
Human Coronary Artery ◽  
Long Chain ◽  
Chain Fatty Acids

Inhibition of Pro-Inflammatory Cytokine Secretion by Select Antioxidants in Human Coronary Artery Endothelial Cells

2020 ◽  
Vol 90 (1-2) ◽  
pp. 103-112 ◽  
Author(s):  
Michael J. Haas ◽  
Marilu Jurado-Flores ◽  
Ramadan Hammoud ◽  
Victoria Feng ◽  
Krista Gonzales ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Ascorbic Acid ◽  
Coronary Artery ◽  
Inflammatory Cytokines ◽  
Inflammatory Cytokine ◽  
Culture Media ◽  
Cytokine Secretion ◽  
Human Coronary Artery ◽  
Tnf Α ◽  
Pro Inflammatory Cytokines

Abstract. Inflammatory and oxidative stress in endothelial cells are implicated in the pathogenesis of premature atherosclerosis in diabetes. To determine whether high-dextrose concentrations induce the expression of pro-inflammatory cytokines, human coronary artery endothelial cells (HCAEC) were exposed to either 5.5 or 27.5 mM dextrose for 24-hours and interleukin-1β (IL-1β), interleukin-2 (IL-2), interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor α (TNF α) levels were measured by enzyme immunoassays. To determine the effect of antioxidants on inflammatory cytokine secretion, cells were also treated with α-tocopherol, ascorbic acid, and the glutathione peroxidase mimetic ebselen. Only the concentration of IL-1β in culture media from cells exposed to 27.5 mM dextrose increased relative to cells maintained in 5.5 mM dextrose. Treatment with α-tocopherol (10, 100, and 1,000 μM) and ascorbic acid (15, 150, and 1,500 μM) at the same time that the dextrose was added reduced IL-1β, IL-6, and IL-8 levels in culture media from cells maintained at 5.5 mM dextrose but had no effect on IL-1β, IL-6, and IL-8 levels in cells exposed to 27.5 mM dextrose. However, ebselen treatment reduced IL-1β, IL-6, and IL-8 levels in cells maintained in either 5.5 or 27.5 mM dextrose. IL-2 and TNF α concentrations in culture media were below the limit of detection under all experimental conditions studied suggesting that these cells may not synthesize detectable quantities of these cytokines. These results suggest that dextrose at certain concentrations may increase IL-1β levels and that antioxidants have differential effects on suppressing the secretion of pro-inflammatory cytokines in HCAEC.

scholarly journals Infection of Human Coronary Artery Endothelial Cells by Group B Streptococcus Contributes to Dysregulation of Apoptosis, Hemostasis, and Innate Immune Responses

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Claudia Beyrich ◽  
Jürgen Löffler ◽  
Anna Kobsar ◽  
Christian P. Speer ◽  
Susanne Kneitz ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Coronary Artery ◽  
Group B Streptococcus ◽  
Gene Array ◽  
Neonatal Morbidity ◽  
Innate Immune ◽  
Human Coronary Artery ◽  
Chemotactic Protein ◽  
Early Onset Sepsis ◽  
Group B

Early onset sepsis due to group B streptococcus leads to neonatal morbidity, increased mortality, and long-term neurological deficencies. Interaction between septicemic GBS and confluent monolayers of human coronary artery endothelial cells (HCAECs) was analyzed by genome wide expression profiling. In total, 124 genes were differentially expressed (89 upregulated, 35 downregulated) based on a more than 3-fold difference to control HCAEC. Regulated genes are involved in apoptosis, hemostasis, oxidative stress response, infection, and inflammation. Regulation of selected genes and proteins identified in the gene array analysis was confirmed by Real-time RT-PCR assay (granulocyte chemotactic protein 2), ELISA (urokinase, cyclooxygenase 2, granulocyte chemotactic protein 1), and western blotting (Heme oxygenase1, BCL2 interacting protein) at various time points between 4 and 24 hours. These results indicate that GBS infection might influence signalling pathways leading to impaired function of the innate immune system and hemorrhagic and inflammatory complications during GBS sepsis.

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