• Molecular & Cellular Toxicology
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• v.5 no.2
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• pp.113-119
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• 2009

Benzo(a)pyrene (BaP) is a persistent environmental contaminant and is present in tobacco smoke. BaP is considered a major contributor of cardiovascular disease. While the activation of endothelial cells by stimuli including tobacco smoke and air pollution contributes importantly to cardiovascular disease, the nature of BaP's mechanism is unclear. In this study, gene expression profiles were investigated in BaPtreated human umbilical vein endothelial cells (HUVECs). Various atherosclerosis related genes could be up- and down-regulated more than 2-fold by BaP, and mRNA levels of atherosclerosis related genes encoding apolipoproteinC III, TLR 2, ICAM 1 and exportin 4 were significantly increased by BaP. Our data suggest that BaP-mediated changes in gene expression contribute to the progression of cardiovascular disease.

• The Journal of the Korean Society for Microbiology
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• v.35 no.2
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• pp.159-169
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• 2000

Scrub typhus is caused by Orientia tsutsugamushi characterized by fever, headache, lymphadenopathy and eschar formation. Infiltration of inflammatory cells around blood vessels and within the affected organs isS known to be pathologic hallmark of the scrub typhus. Recently, expression of adhesion molecules on vascular endothelial cells was implicated as an important pathogenic mechanism in rickettsial disease. This study was performed to examine the expression of adhesion molecules and to investigate its role in the pathogenesis of O. tsutsugamushi infection. The expression of adhesion molecules on human umbilical vein endothelial cells (HUVEC) was measured by flow cytometry and indirect immunofluorescence. Expression of E-selectin, ICAM-1 and VCAM-1 was significantly increased 4 hours after the infection and persisted at least for 24 hours. Expression of those molecules was not induced by killed O. tsutsugamushi. Adhesion of polymorphonuclear cells and mononuclear cells to HUVEC was increased after the infection with O. tsutsugamushi. In conclusion, adhesion molecules are expressed on HUVEC during the infection of live O. tsutsugamushi and those molecules can contribute to the infiltration of inflammatory cells during the infection.

• Biomolecules & Therapeutics
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• v.15 no.3
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• pp.162-168
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• 2007

It is well known that oxidized low-density lipoprotein (oxLDL) is the most characterized humoral factor that plays an important role in the pathogenesis of atherosclerosis. The water extract of the Korean herbal remedy, ZoaGumHwan (ZGH), which is composed of roots of Coptis chinensis Franch and fruits of Evodia officinalis Dode with the ratio of 6 to 1, reduced the in vitro oxidation of low density lipoproteins (LDL). Also, the ZGH extract and berberine, one of the major components of ZGH, significantly prevented oxLDL-induced adhesion of monocytes to human umbilical vein endothelial cells (HUVEC). Furthermore, the ZGH water extract and berberine decreased oxLDL-induced expression of CC chemokine receptor 2 (CCR2), a dominant monocyte chemotaxis receptor, in U937 human monocytic cells. The protective effects of the ZGH water extract and berberine were similar to those of simvastatin, an effective lipid-lowering drug. The results suggest that Korean herbal remedy, ZGH, seems to have protective effect against oxLDL-induced monocyte chemoattractant protein (MCP)-1/CCR2-dependent monocyte recruitment onto endothelial cells.

• International Journal of Oral Biology
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• v.46 no.3
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• pp.99-104
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• 2021

Associations between periodontal infection and cardiovascular disease have been documented. Porphyromonas gingivalis is a well-established periodontal pathogen, and tissue factor (TF) is a key initiator of the coagulation cascade. In this context, P. gingivalis has been reported to enhance TF expression in human endothelial cells. The present study investigated the underlying mechanisms of TF induction by P. gingivalis in human umbilical vein endothelial cells. P. gingivalis increased TF expression in a dose- and time-dependent manner. Not only live bacteria but also glutaraldehyde-fixed bacteria increased TF expression to the same extent. However, sonicates of P. gingivalis did not induce TF expression. Cytochalasin D and SMIFH2, which are inhibitors of actin polymerization and actin nucleation, respectively, inhibited the TF expression induced by P. gingivalis. Finally, TF production was decreased or increased in the presence of various signaling inhibitors, including mitogen-activated protein kinases. These results suggest that P. gingivalis induces endothelial TF expression by a bacterial internalization-dependent mechanism and through diverse signal transduction mechanisms.

• The Korean Journal of Physiology and Pharmacology
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• v.13 no.4
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• pp.301-307
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• 2009

Inflammatory processes of vascular endothelial cells play a key role in the development ofatherosclerosis. We determined the anti-inflammatory effects and mechanisms of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) on LPS-treated human umbilical vein endothelial cells (HUVECs) to evaluate their cardioproteerive potential. Cells were pretreated with DHA, EPA, or troglitazone prior to activation with LPS. Expression of COX-2, prostaglandin $E_2$ ($PGE_2$) and IL-6 production, and $NF-{\kappa}B$ activity were measured by Western blot, ELISA, and luciferase activity, respectively. Results showed that EPA, DHA, or troglitazone significantly reduced COX-2 expression, $NF-{\kappa}B$ luciferase activity, and $PGE_2$ and IL-6 production in a dose-dependent fashion. Interestingly, low doses (10 ${\mu}$M) of DHA and EPA, but not troglitozone, significantly increased the activity of $NF-{\kappa}B$ in resting HUVECs. Our study suggests that while DHA, EPA, and troglitazone may be protective on HUVECs under inflammatory conditions in a dose-dependent manner. However there may be some negative effects when the concentrations are abnormally low, even in normal endothelium.

• Molecules and Cells
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• v.39 no.4
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• pp.292-298
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• 2016

Aquaporin 1 (AQP1) is expressed in most microvasculature endothelial cells and forms water channels that play major roles in a variety of physiologic processes. This study aimed to delineate the transcriptional regulation of AQP1 by Mef2c in endothelial cells. Mef2c cooperated with Sp1 to activate human AQP1 transcription by binding to its proximal promoter in human umbilical cord vein endothelial cells (HUVEC). Over-expression of Mef2c, Sp1, or Mef2c/Sp1 increased HUVEC migration and tube-forming ability, which can be abolished AQP1 knockdown. These data indicate that AQP1 is a direct target of Mef2c in regulating angiogenesis and vasculogenesis of endothelial cells.

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.130.3-131
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• 2003

Inflammation is a frequent radiation-induced following therapeutic irradiation. Since the upregulation of adhesion molecules on endothelial cell surface has been known to be associated with inflammation, interfering with the expression of adhesion molecules is an important therapeutic target. We examined the effect if allicin, a major component of garlic, on the induction of intercellular adhesion molecule-l (ICAM-1) by gamma-irradiation and the mechanisms of its effect in gamma-irradiated human umbilical vein endothelial cells (HUVECs). (omitted)

• Biomolecules & Therapeutics
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• v.25 no.2
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• pp.158-164
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• 2017

Methylglyoxal (MGO) is a highly reactive metabolite of glucose which is known to cause damage and induce apoptosis in endothelial cells. Endothelial cell damage is implicated in the progression of diabetes-associated complications and atherosclerosis. Hypericin, a naphthodianthrone isolated from Hypericum perforatum L. (St. John's Wort), is a potent and selective inhibitor of protein kinase C and is reported to reduce neuropathic pain. In this work, we investigated the protective effect of hypericin on MGO-induced apoptosis in human umbilical vein endothelial cells (HUVECs). Hypericin showed significant anti-apoptotic activity in MGO-treated HUVECs. Pretreatment with hypericin significantly inhibited MGO-induced changes in cell morphology, cell death, and production of intracellular reactive oxygen species. Hypericin prevented MGO-induced apoptosis in HUVECs by increasing Bcl-2 expression and decreasing Bax expression. MGO was found to activate mitogen-activated protein kinases (MAPKs). Pretreatment with hypericin strongly inhibited the activation of MAPKs, including P38, JNK, and ERK1/2. Interestingly, hypericin also inhibited the formation of AGEs. These findings suggest that hypericin may be an effective regulator of MGO-induced apoptosis. In conclusion, hypericin downregulated the formation of AGEs and ameliorated MGO-induced dysfunction in human endothelial cells.

• Journal of the Korean Society of Food Science and Nutrition
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• v.40 no.5
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• pp.635-641
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• 2011

Anti-atherogenic effects in tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$)-stimulated human umbilical vein endothelial cells (HUVEC) are involved with suppressed oxidative stress, cell adhesion molecules, and pro-inflammatory factors. The aim of this study was to determine whether green tea seed coat ethyl acetate fraction (GTSCE) could modulate cell adhesion molecules and inflammatory mediators in HUVEC stimulated with TNF-${\alpha}$. Nitric oxide (NO) production was significantly increased in TNF-${\alpha}$-stimulated HUVEC compared to TNF-${\alpha}$ only treated cells. The NO that is produced by endothelial nitric oxide synthase dilates blood vessels and has protective effects against platelet and leucocyte adhesion. GTSCE at 25, 50, 75, and $100\;{\mu}g$/mL significantly (p<0.05) reduced TNF-${\alpha}$ production. GTSCE significantly (p<0.05) inhibited soluble vascular cell adhesion molecule-1 level, in a dose-dependent manner. Monocyte chemoattractant protein-1 level was also significantly (p<0.05) inhibited by GTSCE treatment at $75\;{\mu}g$/mL compared to the TNF-${\alpha}$-only treated group. Total antioxidant capacity by GTSCE was significantly (p<0.05) enhanced compared to the TNF-${\alpha}$-only treated group. These results suggest that GTSCE can inhibit the production of cell adhesion molecules and inflammatory mediators and could be used as a candidate bioactive material to prevent the development of atherosclerosis.

• Journal of Ginseng Research
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• v.38 no.1
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• pp.34-39
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• 2014

Cigarette smoke is considered a major risk factor for vascular diseases. There are many toxic compounds in cigarette smoke, including acrolein and other ${\alpha},{\beta}$-unsaturated aldehydes, which are regarded as mediators of inflammation and vascular dysfunction. Furthermore, recent studies have revealed that acrolein, an ${\alpha},{\beta}$-unsaturated aldehyde in cigarette smoke, induces inflammatory mediator expression, which is known to be related to vascular diseases. In this study, we investigated whether Korean Red Ginseng (KRG) water extract suppressed acrolein-induced cyclooxygenase (COX)-2 expression in human umbilical vein endothelial cells (HUVECs). Acrolein-induced COX-2 expression was accompanied by increased levels of phosphorylated p38 in HUVECs and KRG inhibited COX-2 expression in HUVECs. These results suggest that KRG suppresses acrolein-induced COX-2 expression via inhibition of the p38 mitogen-activated protein kinase signaling pathway. In addition, KRG exhibited an inhibitory effect on acrolein-induced apoptosis, as demonstrated by annexin Vepropidium iodide staining and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling assay. Consistent with these results, KRG may exert a vasculoprotective effect through inhibition of COX-2 expression in acrolein-stimulated human endothelial cells.