A High Concentration of Melatonin Inhibits In Vitro LDL Peroxidation But Not Oxidized LDL Toxicity Toward Cultured Endothelial Cells

1998 ◽  
Vol 32 (4) ◽  
pp. 582-592 ◽  
Author(s):  
E. Walters-Laporte ◽  
C. Furman ◽  
S. Fouquet ◽  
F. Martin-Nizard ◽  
S. Lestavel ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Oxidized Ldl ◽  
High Concentration ◽  
Cultured Endothelial Cells

Glucose Inhibits Prostacyclin Production by Cultured Aortic Endothelial Cells

1988 ◽  
Vol 60 (02) ◽  
pp. 174-177 ◽  
Author(s):  
Hiroshi Ono ◽  
Fumio Umeda ◽  
Toyoshi Inoguchi ◽  
Hiroshi Ibayashi
Keyword(s):  
Endothelial Cells ◽  
Vascular Wall ◽  
Diabetic Patients ◽  
High Concentration ◽  
Aortic Endothelial Cells ◽  
Cultured Endothelial Cells ◽  
Effect Of Glucose ◽  
Prostacyclin Production ◽  
Aortic Endothelial

SummaryA reduction in production of prostacyclin (PGI2) by the cells in the vascular wall may play a role in the pathogenesis of atherosclerosis in diabetic patients. The present study was undertaken to evaluate the effect of glucose on PGI2 production by endothelial cells in vitro. It was shown that PGI2 production by cultured bovine aortic endothelial cells was significantly reduced in the presence of a high concentration of glucose (300 mg/dl) compared with physiological concentrations of glucose (100 mg/ dl). In contrast, no reduction in PGI2 production was observed in cells cultured with equimolar mannitol, suggesting that glucose itself, rather than the effect of osmolality, inhibited PGI2 production by cultured endothelial cells.In addition, a high concentration of glucose also inhibited the proliferation of cultured endothelial cells.

Histological interaction of cultured endothelial cells and endovascular embolic materials coated with extracellular matrix

1997 ◽  
Vol 86 (1) ◽  
pp. 109-112 ◽  
Author(s):  
Shinichi Tamatani ◽  
Tsunenori Ozawa ◽  
Takashi Minakawa ◽  
Shigekazu Takeuchi ◽  
Tetsuo Koike ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Interventional Treatment ◽  
Clinical Use ◽  
Content Type ◽  
Cultured Endothelial Cells ◽  
Coated Materials ◽  
Embolic Materials ◽  
Polyvinyl Alcohol Particles

✓ This study was undertaken to evaluate the histological reaction of cultured endothelial cells to endovascular embolic materials in vitro. Endothelial cells were isolated and cultured from a canine carotid artery. Embolic materials (platinum microcoils, polyvinyl alcohol particles, silicon balloons, or silk threads), either in their normal state or after having been coated with type 1 collagen, fibronectin, or laminin, were placed on endothelial cells and cocultured for 6, 12, and 24 hours and 2, 3, 7, 14, and 21 days. The cocultures were investigated histologically using a scanning electron microscope. Endothelial cells were not found on any uncoated embolic materials, even at 21 days. On the materials coated with fibronectin or laminin, endothelial cells began to proliferate in 7 days, covering the materials extensively in 14 days. On the other hand, endothelial cells began to proliferate on the collagen-coated materials in 3 days, covering them extensively in 7 days and reaching confluence with a cobblestone pattern in 21 days. The densities of endothelial cells on collagen-coated materials were much higher than those observed on the materials coated with other extracellular matrices. Future advantages of the clinical use of collagen-coated embolic materials in interventional treatment are discussed.

scholarly journals Effects of vitamin E on the toxicity of oxidized LDL on endothelial cells in vitro in smokers vs nonsmokers on diets rich in fish

2005 ◽  
Vol 59 (11) ◽  
pp. 1282-1290 ◽  
Author(s):  
L Seppo ◽  
T Lähteenmäki ◽  
M J Tikkanen ◽  
H Vanhanen ◽  
R Korpela ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Vitamin E ◽  
Oxidized Ldl

scholarly journals Effect of dietary phenolic compounds on apoptosis of human cultured endothelial cells induced by oxidized LDL

1998 ◽  
Vol 123 (3) ◽  
pp. 565-573 ◽  
Author(s):  
Otilia Vieira ◽  
Isabelle Escargueil-Blanc ◽  
Olivier Meilhac ◽  
Jean-Pierre Basile ◽  
Joao Laranjinha ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Phenolic Compounds ◽  
Oxidized Ldl ◽  
Cultured Endothelial Cells

Cultured endothelial cells from distinct vascular areas show differential responses to agonists

1994 ◽  
Vol 72 (9) ◽  
pp. 1007-1012 ◽  
Author(s):  
N. Woodley ◽  
J. K. Barclay
Keyword(s):  
Endothelial Cells ◽  
Nous Avons ◽  
Mots Clés ◽  
Cultured Endothelial Cells ◽  
Differential Responses

Nous avons comparé la capacité des cellules endothéliales isolées de l'aorte, de la veine cave, de la chambre ventriculaire et du système microvasculaire pulmonaire du lapin de produire un ou des facteurs de relaxation en réponse à l'acetylcholine (ACh) et à la bradykinine (BK). Des anneaux aortiques de lapin dépouillés d'endothélium ont été précontractés avec 1 μM de phényléphrine et superfusés à 2 mL/min avec une solution tampon bicarbonatée de Krebs–Henseleit. Les anneaux ont été exposées à des épreuves témoins d'embols de 3 mL de 1 μM d'ACh ou 1 μM de BK. Les embols d'ACh et de BK ont été ajoutés à des cultures de cellules endothéliales qui avaient été incubées pendant 45 min dans des milieux contenant ou non 10 μM de NG-nitro-L-arginine (NNLA). La solution ainsi obtenue a été répandue sur les anneaux en moins de 8 s. Seules les cellules endothéliales ventriculaires gauches stimulées avec ACh et BK et les cellules endothéliales microvasculaires pulmonaires stimulées avec BK ont donné des produits qui ont relaxé les anneaux d'approximativement 6 ± 2%. L'incubation avec la NNLA a atténué ces relaxations. Nos résultats indiquent qu'il existe des différences dans la capacité des cellules endothéliales de divers sites anatomiques de libérer des facteurs de relaxation dérivés de l'oxyde nitrique en réponse à l'ACh et à la BK. Mots clés : facteur de relaxation dérivé de l'endothélium, aorte, dosage biologique in vitro, acétylcholine, bradykinine, superoxyde dismutase, nitroprussiate de sodium.[Traduit par la rédaction]

scholarly journals RIPK1 Expression Associates with Inflammation in Early Atherosclerosis in Humans and Can be Therapeutically Silenced to Reduce NF-κB Activation and Atherogenesis in Mice

Circulation ◽  
2020 ◽  
Author(s):  
Denuja Karunakaran ◽  
My-Anh Nguyen ◽  
Michele Geoffrion ◽  
Dianne Vreeken ◽  
Zachary Lister ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cell Activation ◽  
Inflammatory Responses ◽  
Early Stage ◽  
Oxidized Ldl ◽  
Loss Of Function ◽  
Aortic Sinus ◽  
Atherosclerotic Lesions

Background: Chronic activation of the innate immune system drives inflammation and contributes directly to atherosclerosis. Previously, we showed that macrophages in the atherogenic plaque undergo RIPK3-MLKL-dependent programmed necroptosis in response to sterile ligands such as oxidized LDL and damage-associated patterns (DAMPs) and necroptosis is active in advanced atherosclerotic plaques. Upstream of the RIPK3-MLKL necroptotic machinery lies RIPK1, which acts as a master switch that controls whether the cell undergoes NFκB-dependent inflammation, caspase-dependent apoptosis or necroptosis in response to extracellular stimuli. We therefore set out to investigate the role of RIPK1 in the development of atherosclerosis, which is largely driven by NFκB-dependent inflammation at early stages. We hypothesize that, unlike RIPK3 and MLKL, RIPK1 primarily drives NFκB-dependent inflammation in early atherogenic lesions and knocking down RIPK1 will reduce inflammatory cell activation and protect against the progression of atherosclerosis. Methods: We examined expression of RIPK1 protein and mRNA in both human and mouse atherosclerotic lesions, and using loss-of-function approaches in vitro in macrophages and endothelial cells to measure inflammatory responses. We administered weekly injections of RIPK1 anti-sense oligonucleotides (ASO) to Apoe -/- mice fed a cholesterol-rich (Western) diet for 8 weeks. Results: We find RIPK1 expression is abundant in early-stage atherosclerotic lesions in both humans and mice. Treatment with RIPK1 ASOs led to a reduction in aortic sinus and en face lesion areas (47.2% or 58.8% decrease relative to control, p<0.01) and plasma inflammatory cytokines (IL-1α, IL-17A, p<0.05) compared to controls. RIPK1 knockdown in macrophages decreased inflammatory genes (NFκB, TNFα, IL-1α) and in vivo LPS- and atherogenic diet-induced NF-κB activation. In endothelial cells, knockdown of RIPK1 prevented NF-κB translocation to the nucleus in response to TNFα, where accordingly there was a reduction in gene expression of IL1B, E-selectin and monocyte attachment. Conclusions: We have identified RIPK1 as a central driver of inflammation in atherosclerosis by its ability to activate the NF-κB pathway and promote inflammatory cytokine release. Given the high levels of RIPK1 expression in human atherosclerotic lesions, our study suggests RIPK1 as a future therapeutic target to reduce residual inflammation in patients at high risk of coronary artery disease.

scholarly journals Transcellular biosynthesis of sulfidopeptide leukotrienes during receptor-mediated stimulation of human neutrophil/platelet mixtures

Blood ◽  
1990 ◽  
Vol 76 (9) ◽  
pp. 1838-1844 ◽  
Author(s):  
J Maclouf ◽  
RC Murphy ◽  
PM Henson
Keyword(s):  
Endothelial Cells ◽  
Arachidonic Acid ◽  
Cell Interactions ◽  
Human Neutrophils ◽  
High Concentration ◽  
Opsonized Zymosan ◽  
Leukotriene A4 ◽  
Stimulation Of ◽  
Cell Cell

Abstract The ability of different cell types to cooperate in the metabolism of reactive intermediates of arachidonic acid such as leukotriene A4 (LTA4) is currently receiving considerable attention. Of critical importance is the demonstration that transfer of LTA4 could occur under conditions when relatively low amounts of LTA4 are produced such as would be expected for in vitro receptor-mediated stimulation. Stimulation of human neutrophils with a combination of chemotactic factor (formyl-methionyl-leucyl-phenylalanine, FMLP) and phagocytosable particles (opsonized zymosan) resulted in little production of LTC4 alone, but measurable quantities appeared when platelets were coincubated. When these agonists were added to platelets alone in the absence of neutrophils, no LTC4 was produced. In the presence of stimulated neutrophils, the final synthesis of LTC4 was shown to occur within the platelets (from neutrophil-derived LTA4) by experiments using platelets that had been prelabeled with 35S-cysteine to label intracellular platelet glutathione. Other 35S-labeled sulfidopeptide leukotriene metabolites were also produced in this coincubation of neutrophils and platelets. The observed synergy between FMLP and opsonized zymosan in the production of LTC4 when neutrophils and platelets were coincubated may involve priming the neutrophil for LTA4 production. Activation of platelets or endothelial cells with thrombin did not alter the capacity of either cell to convert exogenously added LTA4 into LTC4. This would support the suggestion that even when platelets are activated they retain their capacity to metabolize LTA4 into LTC4. Finally, previous exposure of the platelets to LTA4 did not affect subsequent metabolism of arachidonic acid by the cyclooxygenase pathway to thromboxane A2 (TXA2) except at very high concentration of LTA4. These results suggest that cell-cell interactions may be critical determinants of the profile of eicosanoids produced in physiologic and pathophysiologic circumstances. In particular, we believe that both endothelial cells and platelets can, together with neutrophils, contribute relatively large amounts of sulfidopeptide leukotrienes to inflammatory and thrombotic events. These cell-cell interactions are aspirin-insensitive; therefore, aspirin-treated platelets are capable of synthesizing the vasoconstrictor LTC4 from neutrophil LTA4 at a time when they can no longer produce thromboxane.

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