scholarly journals c-Src Is the Primary Signaling Mediator of Polychlorinated Biphenyl–Induced Interleukin-8 Expression in a Human Microvascular Endothelial Cell Line

2006 ◽  
Vol 92 (1) ◽  
pp. 311-320 ◽  
Author(s):  
Sung Yong Eum ◽  
Geun Bae Rha ◽  
Bernhard Hennig ◽  
Michal Toborek
Keyword(s):  
Endothelial Cell ◽  
Cell Line ◽  
Polychlorinated Biphenyl ◽  
Interleukin 8 ◽  
Microvascular Endothelial Cell ◽  
Endothelial Cell Line ◽  
Human Microvascular Endothelial Cell ◽  
Microvascular Endothelial

HIF-1 activation attenuates postischemic myocardial injury: role for heme oxygenase-1 in modulating microvascular chemokine generation

2005 ◽  
Vol 289 (2) ◽  
pp. H542-H548 ◽  
Author(s):  
Ramzi Ockaili ◽  
Ramesh Natarajan ◽  
Fadi Salloum ◽  
Bernard J. Fisher ◽  
Drew Jones ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Line ◽  
Heme Oxygenase ◽  
Ischemia Reperfusion ◽  
Microvascular Endothelial Cell ◽  
Endothelial Cell Line ◽  
Human Microvascular Endothelial Cell ◽  
Microvascular Endothelial

The CXC chemokine IL-8, which promotes adhesion, activation, and transmigration of polymorphonuclear neutrophils (PMN), has been associated with production of tissue injury in reperfused myocardium. Hypoxia-inducible factor-1 (HIF-1) is a heterodimeric peptide that is a key regulator of genes such as heme oxygenase (HO)-1 expressed under hypoxic conditions. We hypothesized that HO-1 plays an important role in regulating proinflammatory mediator production under conditions of ischemia-reperfusion. HIF-1 was activated in the human microvascular endothelial cell line (HMEC-1) with the prolyl hydroxylase inhibitor dimethyloxalylglycine (DMOG). DMOG significantly attenuated cytokine-induced IL-8 promoter activity and protein secretion and cytokine-induced PMN migration across human microvascular endothelial cell line HMEC-1 monolayers. In vivo studies in a rabbit model of myocardial ischemia-reperfusion showed that rabbits pretreated with a 20 mg/kg DMOG infusion ( n = 6) 24 h before study exhibited a 21.58 ± 1.76% infarct size compared with 35.25 ± 2.06% in saline-treated ischemia-reperfusion animals ( n = 6, change in reduction = 39%; P < 0.001). In DMOG-pretreated (20 mg/kg) animals, plasma IL-8 levels at 3 h after onset of reperfusion were 405 ± 40 pg/ml vs. 790 ± 40 pg/ml in saline-treated ischemia-reperfusion animals ( P < 0.001). DMOG pretreatment reduced myocardial myeloperoxidase activity, expressed as number of PMN per gram of myocardium, to 1.43 ± 0.59 vs. 4.86 ± 1.1 ( P = 0.012) in saline-treated ischemia-reperfused hearts. Both in vitro and in vivo DMOG-attenuated IL-8 production was associated with robust HO-1 expression. Thus our data show that HIF-1 activation induces substantial HO-1 expression that is associated with attenuated proinflammatory chemokine production by microvascular endothelium in vitro and in vivo.

Hemostatic properties of the SV-40 transfected human microvascular endothelial cell line (HMEC-1)

1995 ◽  
Vol 79 (2) ◽  
pp. 153-161 ◽  
Author(s):  
Maria J.A. Ribeiro ◽  
Donald J. Phillips ◽  
Jane M. Benson ◽  
Bruce L. Evatt ◽  
Edwin W. Ades ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Line ◽  
Microvascular Endothelial Cell ◽  
Endothelial Cell Line ◽  
Human Microvascular Endothelial Cell ◽  
Microvascular Endothelial

Viral susceptibility of an immortalized human microvascular endothelial cell line

1992 ◽  
Vol 39 (1-2) ◽  
pp. 83-90 ◽  
Author(s):  
Edwin W. Ades ◽  
John C. Hierholzer ◽  
Velma George ◽  
Jodi Black ◽  
Francisco Candal
Keyword(s):  
Endothelial Cell ◽  
Cell Line ◽  
Microvascular Endothelial Cell ◽  
Endothelial Cell Line ◽  
Human Microvascular Endothelial Cell ◽  
Viral Susceptibility ◽  
Microvascular Endothelial

HMEC-1: Establishment of an Immortalized Human Microvascular Endothelial Cell Line

1992 ◽  
Vol 99 (6) ◽  
pp. 683-690 ◽  
Author(s):  
Edwin W Ades ◽  
Francisco J Candal ◽  
Robert A Swerlick ◽  
Velma G George ◽  
Susan. Summers ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Cell Line ◽  
Microvascular Endothelial Cell ◽  
Endothelial Cell Line ◽  
Human Microvascular Endothelial Cell ◽  
Microvascular Endothelial

Antigen Presentation by a Continuous Human Microvascular Endothelial Cell Line, HMEC-1 to Human T Cells

Pathobiology ◽  
1993 ◽  
Vol 61 (3-4) ◽  
pp. 236-238 ◽  
Author(s):  
Diane Bosse ◽  
Velma George ◽  
Francisco J. Candal ◽  
Thomas J. Lawley ◽  
Edwin W. Ades
Keyword(s):  
T Cells ◽  
Endothelial Cell ◽  
Antigen Presentation ◽  
Cell Line ◽  
Microvascular Endothelial Cell ◽  
Endothelial Cell Line ◽  
Human Microvascular Endothelial Cell ◽  
Human T Cells ◽  
Microvascular Endothelial

Endothelin-1 production by a microvascular endothelial cell line treated with Plasmodium falciparum parasitized red blood cells

2002 ◽  
Vol 103 (s2002) ◽  
pp. 464S-466S ◽  
Author(s):  
Nicoletta BASILICO ◽  
Livianna SPECIALE ◽  
Silvia PARAPINI ◽  
Pasquale FERRANTE ◽  
Donatella TARAMELLI
Keyword(s):  
Plasmodium Falciparum ◽  
Endothelial Cell ◽  
Red Blood Cells ◽  
Cell Line ◽  
Blood Cells ◽  
Microvascular Endothelial Cell ◽  
Microvascular Endothelium ◽  
Endothelial Cell Line ◽  
Endothelin 1 ◽  
Microvascular Endothelial

In this study, we investigated the production of endothelin 1 (ET-1) by a human microvascular endothelial cell line, HMEC-1, co-cultured with Plasmodium falciparum-parasitized red blood cells (pRBCs). The results indicate that hypoxia increased the basal level of ET-1 production by HMEC-1 cells after 24 or 48h of treatment. However, the co-incubation of HMEC-1 cells with pRBCs, but not with uninfected RBCs, induced a dose-dependent decrease of both constitutive and hypoxia-induced ET-1 production. The inhibition was not due to a decrease in cell viability, as lactate dehydrogenase release remained constant. These results indicate that pRBCs are able to interfere with both the constitutive and stimulated ET-1 release from the microvascular endothelium, thus inducing local modifications of the vascular tone and of the inflammatory response. This could be of relevance in the pathogenesis of the most severe forms of P. falciparum infections, such as cerebral malaria or malaria during pregnancy.

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