Anti-inflammatory properties of kaempferol via its inhibition of aldosterone signaling and aldosterone-induced gene expression

2014 ◽  
Vol 92 (2) ◽  
pp. 117-123 ◽  
Author(s):  
Zi-Kui Liu ◽  
Hong-Bo Xiao ◽  
Jun Fang
Keyword(s):  
Gene Expression ◽  
Endothelial Cells ◽  
Inflammatory Cytokine ◽  
Umbilical Vein ◽  
Binding Activity ◽  
Flavonoid Compound ◽  
Oxygen Species ◽  
Anti Inflammatory ◽  
Umbilical Vein Endothelial Cells ◽  
Cluster Of Differentiation

Osteopontin (OPN), also called cytokine Eta-1, is a pro-inflammatory cytokine. Recent studies have shown that aldosterone increases OPN gene expression in endothelial cells. As a flavonoid compound, kaempferol has potent anti-inflammatory properties, but whether kaempferol regulates aldosterone signaling and aldosterone-induced gene expression is still unknown. Human umbilical vein endothelial cells (HUVECs) were pretreated with kaempferol (0, 1, 3, or 10 μmol/L) for 1 h prior to exposure to aldosterone (10−6 mol/L) for 24 h. Aldosterone induced generation of reactive oxygen species; OPN and cluster of differentiation 44 gene expression; phospho-p38 MAPK and NF-κB binding activity. The effect of aldosterone was abrogated by kaempferol and spironolactone (10−6 mol/L). The present results suggest that kaempferol exerts its anti-inflammatory properties via its inhibition of aldosterone signaling and aldosterone-induced gene expression in HUVECs.

Prolonged shear stress and KLF2 suppress constitutive proinflammatory transcription through inhibition of ATF2

Blood ◽  
2007 ◽  
Vol 109 (10) ◽  
pp. 4249-4257 ◽  
Author(s):  
Joost O. Fledderus ◽  
Johannes V. van Thienen ◽  
Reinier A. Boon ◽  
Rob J. Dekker ◽  
Jakub Rohlena ◽  
...  
Keyword(s):  
Gene Expression ◽  
Endothelial Cells ◽  
Shear Stress ◽  
Umbilical Vein ◽  
Expression Profiles ◽  
Binding Activity ◽  
Tnf Α ◽  
Proinflammatory Gene ◽  
Umbilical Vein Endothelial Cells ◽  
Proinflammatory Gene Expression

Abstract Absence of shear stress due to disturbed blood flow at arterial bifurcations and curvatures leads to endothelial dysfunction and proinflammatory gene expression, ultimately resulting in atherogenesis. KLF2 has recently been implicated as a transcription factor involved in mediating the anti-inflammatory effects of flow. We investigated the effect of shear on basal and TNF-α–induced genomewide expression profiles of human umbilical vein endothelial cells (HUVECs). Cluster analysis confirmed that shear stress induces expression of protective genes including KLF2, eNOS, and thrombomodulin, whereas basal expression of TNF-α–responsive genes was moderately decreased. Promoter analysis of these genes showed enrichment of binding sites for ATF transcription factors, whereas TNF-α–induced gene expression was mostly NF-κB dependent. Furthermore, human endothelial cells overlying atherosclerotic plaques had increased amounts of phosphorylated nuclear ATF2 compared with endothelium at unaffected sites. In HUVECs, a dramatic reduction of nuclear binding activity of ATF2 was observed under shear and appeared to be KLF2 dependent. Reduction of ATF2 with siRNA potently suppressed basal proinflammatory gene expression under no-flow conditions. In conclusion, we demonstrate that shear stress and KLF2 inhibit nuclear activity of ATF2, providing a potential mechanism by which endothelial cells exposed to laminar flow are protected from basal proinflammatory, atherogenic gene expression.

scholarly journals Ethanol inhibits monocyte chemotactic protein-1 expression in interleukin-1β-activated human endothelial cells

2005 ◽  
Vol 289 (4) ◽  
pp. H1669-H1675 ◽  
Author(s):  
John P. Cullen ◽  
Shariq Sayeed ◽  
Ying Jin ◽  
Nicholas G. Theodorakis ◽  
James V. Sitzmann ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Binding Activity ◽  
Protective Effects ◽  
Monocyte Adhesion ◽  
Monocyte Chemotactic Protein ◽  
Chemotactic Protein ◽  
Subendothelial Space ◽  
Umbilical Vein Endothelial Cells

The aim of this study was to determine the effect of ethanol (EtOH) on endothelial monocyte chemotactic protein-1 (MCP-1) expression. IL-1β increased the production of MCP-1 by human umbilical vein endothelial cells from undetectable levels to ∼900 pg/ml at 24 h. EtOH dose-dependently inhibited IL-1β-stimulated MCP-1 secretion as determined by ELISA: 25 ± 1%, 35 ± 7%, and 65 ± 5% inhibition for 1, 10, and 100 mM EtOH, respectively, concomitant with inhibition of monocyte adhesion to activated endothelial cells. Similarly, EtOH dose-dependently inhibited IL-1β-stimulated MCP-1 mRNA expression. Experiments with actinomycin D demonstrated that EtOH decreased the stability of MCP-1 mRNA. In addition, EtOH significantly reduced NF-κB and AP-1 binding activity induced by IL-1β and inhibited MCP-1 gene transcription. Binding of 125I-labeled MCP-1 to its receptor (CCR2) on THP-1 human monocytic cells was not affected by EtOH treatment. Modulation of the expression of MCP-1 represents a mechanism whereby EtOH could inhibit atherogenesis by blocking the crucial early step of monocyte adhesion and subsequent recruitment to the subendothelial space. These actions of EtOH may underlie, in part, its cardiovascular protective effects in vivo.

scholarly journals Dengue Virus Induces Novel Changes in Gene Expression of Human Umbilical Vein Endothelial Cells

2003 ◽  
Vol 77 (21) ◽  
pp. 11822-11832 ◽  
Author(s):  
Rajas V. Warke ◽  
Kris Xhaja ◽  
Katherine J. Martin ◽  
Marcia F. Fournier ◽  
Sunil K. Shaw ◽  
...  
Keyword(s):  
Gene Expression ◽  
Endothelial Cells ◽  
Dengue Virus ◽  
Immune Cell ◽  
Umbilical Vein ◽  
Oligoadenylate Synthetase ◽  
Functional Responses ◽  
Human Umbilical Vein ◽  
Phospholipid Scramblase ◽  
Umbilical Vein Endothelial Cells

ABSTRACT Endothelial cells are permissive to dengue virus (DV) infection in vitro, although their importance as targets of DV infection in vivo remains a subject of debate. To analyze the virus-host interaction, we studied the effect of DV infection on gene expression in human umbilical vein endothelial cells (HUVECs) by using differential display reverse transcription-PCR (DD-RTPCR), quantitative RT-PCR, and Affymetrix oligonucleotide microarrays. DD identified eight differentially expressed cDNAs, including inhibitor of apoptosis-1, 2′-5′ oligoadenylate synthetase (OAS), a 2′-5′ OAS-like (OASL) gene, galectin-9, myxovirus protein A (MxA), regulator of G-protein signaling, endothelial and smooth muscle cell-derived neuropilin-like protein, and phospholipid scramblase 1. Microarray analysis of 22,000 human genes confirmed these findings and identified an additional 269 genes that were induced and 126 that were repressed more than fourfold after DV infection. Broad functional responses that were activated included the stress, defense, immune, cell adhesion, wounding, inflammatory, and antiviral pathways. These changes in gene expression were seen after infection of HUVECs with either laboratory-adapted virus or with virus isolated directly from plasma of DV-infected patients. Tumor necrosis factor alpha, OASL, and MxA and h-IAP1 genes were induced within the first 8 to 12 h after infection, suggesting a direct effect of DV infection. These global analyses of DV effects on cellular gene expression identify potentially novel mechanisms involved in dengue disease manifestations such as hemostatic disturbance.

scholarly journals Evaluation of Anti-Inflammatory Components of Guizhi Fuling Capsule, an Ancient Chinese Herbal Formula, in Human Umbilical Vein Endothelial Cells

2020 ◽  
Vol 2020 ◽  
pp. 1-8 ◽  
Author(s):  
Yuzhong Zheng ◽  
Guizhong Xin ◽  
Guowei Gong ◽  
Tina TX Dong ◽  
Ping Li ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Active Components ◽  
Human Umbilical Vein ◽  
Cellular Inflammation ◽  
Cyclooxygenase 1 ◽  
Cox 2 ◽  
Anti Inflammatory ◽  
Umbilical Vein Endothelial Cells ◽  
Cox 1

Background. Guizhi Fuling capsule (GFC), a well-known formula composed of five medicinal herbs, is commonly prescribed to treat primary dysmenorrhea, as well as to achieve good clinical efficacy in China. However, the active components of GFC have not been identified. Here, the anti-inflammatory functions of GFC, as well as its major ingredients, were evaluated in human umbilical vein endothelial cells (HUVECs). Methods. Lipopolysaccharide (LPS) was used in HUVECs to imitate the cellular inflammation. Then, GFC-triggered mRNA expressions of cyclooxygenase-1 (COX-1) and COX-2 were determined by real-time PCR, while the expression of COX-2 protein was revealed by western blotting. Besides, nine components of GFC were evaluated for their contribution value in the anti-dysmenorrhea effects Results. The application of GFC downregulated the mRNA expressions of COX-1 and COX-2 mRNAs. Nine major components of GFC were tested in the inflammatory system, and three compounds, including paeoniflorin, benzoylpaeoniflorin, and amygdalin, exhibited robust activation in HUVECs. The combination of paeoniflorin, benzoylpaeoniflorin, and amygdalin showed over 80% of the anti-inflammatory activation. Conclusion. Our study supports that GFC plays a promising role in anti-dysmenorrhea function by decreasing COXs’ expression. Besides, paeoniflorin, benzoylpaeoniflorin, and amygdalin could be considered as major regulators for the anti-dysmenorrhea effects of GFC.

scholarly journals In vitro effects of low-level aldehyde exposures on human umbilical vein endothelial cells

2015 ◽  
Vol 4 (5) ◽  
pp. 1250-1259 ◽  
Author(s):  
Nuan P. Cheah ◽  
Jeroen L.A. Pennings ◽  
Jolanda P. Vermeulen ◽  
Roger W.L. Godschalk ◽  
Frederik J. van Schooten ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cardiovascular Disease ◽  
Endothelial Cells ◽  
Tobacco Smoke ◽  
Umbilical Vein ◽  
Human Umbilical Vein ◽  
In Vitro Effects ◽  
Umbilical Vein Endothelial Cells ◽  
Disease Exposure

Aldehydes cause gene expression changes for genes associated with cardiovascular disease. Exposure to aldehydes from tobacco smoke needs to be controlled.

scholarly journals Enhancement by Hydrogen Peroxide of Calcium Signals in Endothelial Cells Induced by 5-HT1B and 5-HT2B Receptor Agonists

2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
Pavel V. Avdonin ◽  
Alexander D. Nadeev ◽  
Galina Yu. Mironova ◽  
Irina L. Zharkikh ◽  
Piotr P. Avdonin ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Endothelial Cells ◽  
Calcium Ions ◽  
Umbilical Vein ◽  
Oxygen Species ◽  
Calcium Signals ◽  
Vasodilatory Effect ◽  
Umbilical Vein Endothelial Cells ◽  
Endothelium Dependent Relaxation

Hydrogen peroxide, formed in the endothelium, acts as a factor contributing to the relaxation of blood vessels. The reason for this vasodilatory effect could be modulation by H2O2 of calcium metabolism, since mobilization of calcium ions in endothelial cells is a trigger of endothelium-dependent relaxation. The aim of this work was to investigate the influence of H2O2 on the effects of Ca2+-mobilizing agonists in human umbilical vein endothelial cells (HUVEC). We have found that H2O2 in concentration range 10-100 μM increases the rise of [Ca2+]i induced by 5-hydroxytryptamine (5-HT) and carbachol and does not affect the calcium signals of ATP, agonist of type 1 protease-activated receptor SFLLRN, histamine and bradykinin. Using specific agonists of 5-HT1B and 5-HT2B receptors CGS12066B and BW723C86, we have demonstrated that H2O2 potentiates the effects mediated by these types of 5-HT receptors. Potentiation of the effect of BW723C86 can be produced by the induction of endogenous oxidative stress in HUVEC. We have shown that the activation of 5-HT2B receptor by BW723C86 causes production of reactive oxygen species (ROS). Inhibitor of NADPH oxidases VAS2870 suppressed formation of ROS and partially inhibited [Ca2+]i rise induced by BW723C86. Thus, it can be assumed that vasorelaxation induced by endogenous H2O2 in endothelial cells partially occurs due to the potentiation of the agonist-induced calcium signaling.

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