Stimulation of serglycin and CD44 mRNA expression in endothelial cells exposed to TNF-α and IL-1α

1999 ◽  
Vol 1428 (2-3) ◽  
pp. 225-232 ◽  
Author(s):  
Mari Ann Kulseth ◽  
Svein Olav Kolset ◽  
Trine Ranheim
Keyword(s):  
Endothelial Cells ◽  
Mrna Expression ◽  
Tnf Α ◽  
Stimulation Of

Abstract 191: NF-?B p65 Methylation by Protein Arginine Methyltransferase 5 (PRMT5) is Necessary for the Transcriptional Induction of CXCL10 by TNF-a

2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Daniel P Harris
Keyword(s):  
Endothelial Cells ◽  
Mrna Expression ◽  
Chromatin Immunoprecipitation ◽  
Proximal Promoter ◽  
Protein Arginine Methyltransferase ◽  
Arginine Methyltransferase ◽  
Expression Of Genes ◽  
Tnf Α ◽  
Affect Expression ◽  
Transcriptional Induction

TNF-α initiates the expression of genes involved in the recruitment, adhesion, and transmigration of leukocytes to sites of inflammation. Here, we report that the protein arginine methyltransferase PRMT5 is required for the transcriptional induction of the pro-inflammatory chemokine CXCL10 (IP-10) in endothelial cells. Depletion of PRMT5 by siRNA results in significantly diminished TNF-α-induced CXCL10 mRNA expression, but does not affect expression of other chemokines, such as MCP-1 or IL-8. Chromatin immunoprecipitation experiments of the CXCL10 proximal promoter show the presence of symmetrical dimethylated arginine (sDMA)-containing proteins upon exposure to TNF-α. This methylation is completely lost when PRMT5 is removed from cells by siRNA. Using immunoprecipitation, we show that PRMT5 enhances CXCL10 expression by methylating the RelA (p65) subunit of NF-κB. In summary, we have identified that PRMT5 is a novel regulator of CXCL10 expression. Further, we have discovered that PRMT5 methylates NF-κB, a finding which may further knowledge of the post-translational code governing NF-κB regulation and target specificity.

scholarly journals Immune Disorders of Dentoalveolar Anomalies in Schoolchildren

2019 ◽  
pp. 1-5
Author(s):  
Olimov Siddik Sharifovich
Keyword(s):  
Endothelial Cells ◽  
Systemic Inflammatory Response Syndrome ◽  
Inflammatory Response ◽  
Lymphoid Cell ◽  
Oral Fluid ◽  
Immune Disorders ◽  
Tnf Α ◽  
Α Level ◽  
Adaptive Reactions ◽  
Stimulation Of

Increasing in IL-1, IL-6, IL-8 and TNF-α level in blood and oral fluid indicates an increase in antigenic stimulation of monocyte-macrophage, lymphoid cell elements, endothelial cells, fibroblasts of various organs and tissues, specifies systemic inflammatory response syndrome development and protective-adaptive reactions and maladaptation reactions formation at children with DAA.

scholarly journals Heme induces mRNA expression and activation of tissue factor by TLR4 dependent mechanisms

2020 ◽  
Author(s):  
B.W. Hounkpe ◽  
C.R.P. Moraes ◽  
M.N.N. do Santos ◽  
F. F. Costa ◽  
E.V. De Paula
Keyword(s):  
Endothelial Cells ◽  
Mrna Expression ◽  
Tissue Factor ◽  
Mononuclear Cells ◽  
Cell Disease ◽  
Coagulation Activation ◽  
Coagulation Activity ◽  
Human Mononuclear Cells ◽  
Tnf Α ◽  
Dependent Pathway

AbstractIntroductionHemolytic diseases such as Sickle Cell Disease (SCD) are characterized by a natural propensity for both arterial and venous thrombosis. Evidence showing that heme can induce tissue factor (TF) expression in endothelial cells and TF-dependent coagulation activation in animal models of SCD suggest that heme can contribute to hypercoagulability in this condition. We recently demonstrated that heme can induce coagulation activation in whole blood of healthy volunteers in a TF-dependent fashion.MethodsHerein, we aimed to evaluate whether this heme-induced coagulation activity was dependent on the expression and/or activation of hematopoietic TF in human mononuclear cells. TF mRNA expression was evaluated by qPCR and TF procoagulant activity was evaluated using a 2-stage assay based on the generation of FXa.ResultsHeme was capable of inducing TF expression and activation in a TLR4-dependent pathway. This activity was further amplified after TNF-α-priming.ConclusionOur results provide additional evidences on the mechanisms by which heme is involved in the pathogenesis of hypercoagulability in hemolytic diseases.

DIFFERENTIAL EFFECTS OF SHEAR STRESS ON THE EXPRESSIONS OF ICAM-1 AND VCAM-1 INDUCED BY TNF-α IN ENDOTHELIAL CELLS

2005 ◽  
Vol 05 (01) ◽  
pp. 63-79
Author(s):  
JENG-JIANN CHIU ◽  
PEI-LING LEE ◽  
SHUNICHI USAMI ◽  
SHU CHIEN
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Mrna Expression ◽  
Adhesion Molecule ◽  
Vascular Endothelial Cells ◽  
Surface Protein ◽  
Intercellular Adhesion Molecule ◽  
Intercellular Adhesion Molecule 1 ◽  
Induced Expression ◽  
Tnf Α

Vascular endothelial cells (ECs) are subjected to shear stress and cytokine stimulation. We studied the interplay between shear stress and cytokine in modulating the expression of adhesion molecule genes and the adhesive function of ECs. Shear stress (20 dynes/cm2) was applied to ECs prior to or following the addition of tumor necrosis factor (TNF)-α. Shear stress increased the TNF-α-induced expression of intercellular adhesion molecule-1 (ICAM-1) at both mRNA and surface protein levels, but decreased the TNF-α-induced expression of vascular adhesion molecule-1 (VCAM-1). The TNF-α-induced increase in EC adhesiveness for monocytic THP-1 cells was reduced by shear stress. After 24-h pre-shearing followed by 1 h of static incubation, the effect of pre-shearing on TNF-α-induced ICAM-1 mRNA expression vanished. The recovery of the TNF-α-induced VCAM-1 mRNA expression following pre-shearing, however, required a static incubation time of >6 h (completely recovery at 24 h). Pre- and post-shearing caused a reduction in the nuclear factor (NF)-κB-DNA binding activity induced by TNF-α in the EC nucleus. Our findings suggest that shear stress plays differential roles in modulating the TNF-α-induced EC expressions of ICAM-1 and VCAM-1 genes, which serve similar functions in vascular biology.

Adiponectin inhibits tissue factor expression and enhances tissue factor pathway inhibitor expression in human endothelial cells

2008 ◽  
Vol 100 (08) ◽  
pp. 291-300 ◽  
Author(s):  
Yi-Jian Chen ◽  
Li-Qun Zhang ◽  
Guang-Ping Wang ◽  
Hui Zeng ◽  
Ben Lü ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Protein Expression ◽  
Mrna Expression ◽  
Tissue Factor ◽  
Tissue Factor Pathway Inhibitor ◽  
Inhibitory Effect ◽  
Dependent Manner ◽  
Tnf Α ◽  
Tissue Factor Pathway ◽  
Expression And Activity

SummaryTissue factor (TF) plays a pivotal role in thrombus formation and atherogenesis in acute coronary syndrome. Tissue factor pathway inhibitor (TFPI) is a specific physiological inhibitor of TF/ FVIIa complex that regulates TF-induced coagulation. Adiponectin (Adp) is an adipocyte-specific adipocytokine with anti-atherogenic and anti-diabetic properties. Adp inhibits inflammatory cytokine and adhesion molecules expression, and it can prevent endothelial dysfunction. In this study, we investigated the effects of Adp on tumor necrosis factor-α (TNF-α)-induced expression of TF and TFPI in human umbilical vein endothelial cells (HU-VECs), and the signaling transduction pathways involved. It was found that Adp significantly inhibited both TF protein expression and activity in TNF-α-stimulated HUVECs. In the meanwhile, it increased TFPI protein expression and activity for about two folds. Adp also inhibited TF mRNA expression induced by TNF-α, but had no effect on TFPI mRNA expression. The inhibitory effect of Adp onTNF-α-inducedTF expression was prevented by pretreatment with Rp-cAMPs, a PKA inhibitor. Adp increased intracellular cAMP content and PKA activity levels in a dose-dependent manner. Phosphorylation of IκB-α was decreased by Adp, but phosphorylation of p44/42MAPK, SAPK/ JNK, and p38MAPK were not affected. These results suggested that Adp inhibits TF expression through inhibition of a PKA dependent nuclear factor- κB (NF-κB) signaling pathway. It was also found that adiponectin promoted Akt and AMP-activated protein kinase phosphorylation. The inhibitory effect of Adp on TNF-α-induced TF synthesis was abrogated in part by pretreatment with the PI3kinase inhibitor LY 294002, suggesting that Akt activation might inhibit TF expression induced by TNF-α. The inhibitory effect of Adp is almost completely abrogated by inhibition of both the cAMP/PKA pathway and PI3K/Akt pathway. In conclusion, our data indicated that inhibition of NF-κB through stabilization of IκB-α and activation of Akt phosphorylation may mediate the inhibitory effect of Adp on TF expression; but the enhancement effect of Adp on the TFPI production might occur via translational rather than transcriptional regulation.

Regulation of endothelin synthesis in hepatic endothelial cells

1998 ◽  
Vol 274 (6) ◽  
pp. G1068-G1076 ◽  
Author(s):  
Ann T. Eakes ◽  
Merle S. Olson
Keyword(s):  
Endothelial Cells ◽  
Mrna Expression ◽  
Kupffer Cells ◽  
Transforming Growth Factor ◽  
Culture Media ◽  
Mrna Level ◽  
Endotoxin Challenge ◽  
Endotoxin Exposure ◽  
Tnf Α ◽  
Liver Endothelial Cells

Endothelin (ET) stimulates vasoconstriction and glucose production and mediator synthesis in the liver. Only hepatic endothelial cells express ET-1 mRNA, and during endotoxemia in the intact rat, a ninefold increase in hepatic ET-1 mRNA occurs within 3 h of lipopolysaccharide (LPS) infusion [A. T. Eakes, K. M. Howard, J. E. Miller, and M. S. Olson. Am. J. Physiol. 272 ( Gastrointest. Liver Physiol. 35): G605–G611, 1997]. The present study defines the mechanism by which hepatic ET production is enhanced during endotoxin exposure. Culture media conditioned by exposure to endotoxin-treated Kupffer cells stimulated a twofold increase in immunoreactive ET-1 (irET-1) secretion by liver endothelial cells. Transforming growth factor-β (TGF-β), tumor necrosis factor-α (TNF-α), LPS, and platelet-activating factor (PAF) were tested for their ability to stimulate cultured liver endothelial cells to secrete irET-1. Although TNF-α, LPS, and PAF had no significant effect on ET-1 synthesis, TGF-β increased ET-1 mRNA expression and irET-1 secretion. In coculture experiments, treating Kupffer cells with endotoxin caused a doubling of the ET-1 mRNA level in the liver endothelial cells. This increase in ET-1 mRNA was attenuated by a TGF-β-neutralizing antibody. Hence, a paracrine signaling mechanism operates between Kupffer cells that release TGF-β on endotoxin challenge and hepatic endothelial cells in which TGF-β stimulates ET-1 mRNA expression and ET-1 secretion; this intercellular signaling relationship is an important component in the hepatic responses to endotoxin exposure.

Abstract 268: Adiponectin Ameliorates Palmitate Acid Induced Endothelial Inflammation in Endothelial Cells

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Xiuping Chen ◽  
Wenwen Zhao ◽  
Xuenong Zhang ◽  
Chuanhong Wu
Keyword(s):  
Endothelial Cells ◽  
Cardiovascular Diseases ◽  
Endothelial Dysfunction ◽  
Protein Expression ◽  
Mrna Expression ◽  
Technology Development ◽  
Umbilical Vein ◽  
Early Event ◽  
Development Fund ◽  
Tnf Α

Endothelial dysfunction (ED) is considered an early event of cardiovascular diseases including hypertension, atherosclerosis and so on. Inflammation participates centrally in all stages of cardiovascular diseases and is considered as a hallmark of endothelial dysfunction. In this study, the effect of adiponectin (APN), an adipocytokine derived mainly from adipocytes, on palmitate acid (PA)-induced inflammation in endothelial cells. Human umbilical vein endothelial cells (HUVECs) were treated with PA with or without APN pretreatment. The mRNA expression of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and ICAM-1 were measured with RT-PCR. The protein expression of ICAM-1, NOX1, NOX2, NOX4, and phosphorylation of MAPKs (JNK, ERK, and p38MAPK), IKKβ, p65 NF-κB were determined by Western blotting. Intracellular reactive oxygen species (ROS) and nitric oxide (NO) formation were determined with DCFH2-DA and DAF-FM respectively. APN significantly ameliorated PA-induced mRNA expression of TNF-α, IL-6 and ICAM-1 and protein expression of ICAM-1, NOX2, and phosphorylation of IKKβ, p65 NF-κB, p38MAPK, without affecting NOX2 and phosphorylation of JNK and ERK. APN also partly reversed PA induced ROS formation and NO decrease. NAC, a ROS scavenger, showed similar activities. The p38MAK inhibitor, SB203580, also reversed PA induced protein expression of ICAM-1 and mRNA expression of TNF-α, IL-6 and ICAM-1. Taken together, these results showed that APN improved PA induced endothelial dysfunction by regulating ROS/p38MAK/NF-κB pathways. Acknowledgement: This study was supported by the National Natural Science Foundation of China (No. 81160048) and the Science and Technology Development Fund of Macau Special Administrative Region (No. 021/2012/A1).

Two-way arginine transport in human endothelial cells: TNF-α stimulation is restricted to system y+

2002 ◽  
Vol 282 (1) ◽  
pp. C134-C143 ◽  
Author(s):  
Roberto Sala ◽  
Bianca Maria Rotoli ◽  
Emanuela Colla ◽  
Rossana Visigalli ◽  
Alessandro Parolari ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Nitric Oxide Synthase ◽  
Umbilical Vein ◽  
Nitrite Accumulation ◽  
Arginine Transport ◽  
Tnf Α ◽  
Umbilical Vein Endothelial Cells ◽  
Oxide Synthase ◽  
Stimulation Of

Human umbilical vein endothelial cells transport arginine through two Na+-independent systems. System y+L is insensitive to N-ethylmaleimide (NEM), inhibited byl-leucine in the presence of Na+, and referable to the expression of SLC7A6/y+LAT2, SLC7A7/y+LAT1, and SLC3A2/4F2hc. System y+ is referable to the expression of SLC7A1/CAT1 and SLC7A2/CAT2B. Tumor necrosis factor-α (TNF-α) and bacterial lipopolysaccharide induce a transient stimulation of arginine influx and efflux through system y+. Increased expression of SLC7A2/CAT2B is detectable from 3 h of treatment, while SLC7A1 expression is inhibited at later times of incubation. System y+L activity and expression remain unaltered. Nitric oxide synthase type 2 mRNA is not detected in the absence or presence of TNF-α, while the latter condition lowers nitric oxide synthase type 3 expression at the mRNA and the protein level. Nitrite accumulation is comparable in cytokine-treated and control cells up to 48 h of treatment. It is concluded that modulation of endothelial arginine transport by TNF-α or lipopolysaccharide occurs exclusively through changes in CAT2B and CAT1 expression and is dissociated from stimulation of nitric oxide production.

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.

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