<i>Borrelia Burgdorferi</i>Upregulates the Adhesion Molecules E-selectin, P-selectin, ICAM-1 and VCAM-1 on Mouse Endothelioma Cells<i>in vitro</i>

Böggemeyer, Elena; Stehlé, Thomas; Schaible, Ulrich E.; Hahne, Michael; Vestweber, Dietmar; Simon, Markus M.

doi:10.3109/15419069409004433

Cited by 51 publications

(27 citation statements)

References 53 publications

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“…Endothelial cells also direct migrating cells into the tissue via the upregulation of adhesion molecules, such as VCAM-1, ICAM-1, and E-selectin. Thus, autoimmune reactions and B. burgdorferi, C. pneumoniae, and cytomegalovirus infections all increase the expression of VCAM-1, ICAM-1, and E-selectin in endothelial cells (8,19,32). A previous study by Hatz et al (27) showed that individuals suffering from H. pylori-associated antral gastritis have increased expression of VCAM-1 and ICAM-1 on endothelial cells, but they did not find any E-selectin expression.…”

Section: Discussionmentioning

confidence: 97%

Helicobacter pylori-Induced Activation of Human Endothelial Cells

et al. 2002

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Helicobacter pylori infection causes active chronic inflammation with a continuous recruitment of neutrophils to the inflamed gastric mucosa. To evaluate the role of endothelial cells in this process, we have examined adhesion molecule expression and chemokine and cytokine production from human umbilical vein endothelial cells stimulated with well-characterized H. pylori strains as well as purified proteins. Our results indicate that endothelial cells actively contribute to neutrophil recruitment, since stimulation with H. pylori bacteria induced upregulation of the adhesion molecules VCAM-1, ICAM-1, and E-selectin as well as the chemokines interleukin 8 (IL-8) and growth-related oncogene alpha (GRO-␣) and the cytokine IL-6. However, there were large variations in the ability of the different H. pylori strains to stimulate endothelial cells. These interstrain variations were seen irrespective of whether the strains had been isolated from patients with duodenal ulcer disease or asymptomatic carriers and were not solely related to the expression of known virulence factors, such as the cytotoxin-associated gene pathogenicity island, vacuolating toxin A, and Lewis blood group antigens. In addition, one or several unidentified proteins which act via NF-B activation seem to induce endothelial cell activation. In conclusion, human endothelial cells produce neutrophil-recruiting factors and show increased adhesion molecule expression after stimulation with certain H. pylori strains. These effects probably contribute to the continuous recruitment of neutrophils to H. pylori-infected gastric mucosa and may also contribute to tissue damage and ulcer formation.

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Section: Discussionmentioning

confidence: 97%

Helicobacter pylori-Induced Activation of Human Endothelial Cells

et al. 2002

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“…The increased expression of adhesion molecules such as intracellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), E-selectin, and P-selectin has been demonstrated upon in vitro interaction of B. burgdorferi and host endothelial tissues (19). The joint tissues of B. burgdorferi-infected mice also have been shown to significantly upregulate the expression of these adhesion molecules (127).…”

Section: Development Of Arthritis Upon Infection With B Burgdorferimentioning

confidence: 92%

Lyme Arthritis: Current Concepts and a Change in Paradigm

Nardelli

Callister

Schell

2008

Clin Vaccine Immunol

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“…To investigate how hypoxia and ischemia regulate endoglin expression in cerebral microvascular endothelial cells and to determine which signaling pathways are involved, we examined expression of endoglin mRNA and protein in hypoxic bEND.3 mouse brain capillary endothelial cells and in focal cerebral ischemia in mice. bEND.3 cells exhibit endothelial properties, including expression of von Willebrand factor (vWF), 15 vascular endothelial growth factor receptors, 15 E-selectin, 16 platelet-endo-thelial cell adhesion molecule-1, 17 vascular cell adhesion molecule-1, 18 mucosal vascular addressin cell adhesion molecule-1, 18 endothelial NO synthase, 19 and endomucin. 20 bEND.3 cells can internalize acetylated low-density lipoprotein and produce capillary-like tubes in 3-dimensional cultures.…”

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confidence: 99%

Hypoxic Induction of Endoglin via Mitogen-Activated Protein Kinases in Mouse Brain Microvascular Endothelial Cells

Zhu

Sun

Xie

et al. 2003

Stroke

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Background and Purpose-Endoglin (CD105) is a membrane glycoprotein that is mutated in hereditary hemorrhagic telangiectasia (Osler-Rendu-Weber disease) and shows increased expression in proliferating endothelial cells during angiogenesis. Methods-We investigated the effect of hypoxia on endoglin expression in murine cerebral microvascular endothelial (bEND.3) cells in vitro and the possible involvement of mitogen-activated protein kinase (MAPK) pathways. Results-Hypoxia increased endoglin mRNA and protein expression in bEND.3 cells, which was associated with phosphoactivation of extracellular signal-related kinase (ERK), p38 MAPK, and Jun amino-terminal kinase (JNK).Inhibitors of p38 decreased hypoxic induction of endoglin expression, as did dominant negative MAPK kinase 3 (MKK3), which activates p38. In contrast, constitutively active MKK3 or JNK1 potentiated the hypoxic induction of endoglin. Conclusions-These results indicate that hypoxia induces the expression of endoglin at both the mRNA and protein levels and that induction is regulated by the p38 and perhaps also JNK pathways. Key Words: angiogenesis Ⅲ brain Ⅲ endoglin Ⅲ endothelium Ⅲ hypoxia Ⅲ mitogen-activated protein kinases Ⅲ protein kinases H ypoxia-induced angiogenesis increases blood flow and oxygen delivery to ischemic tissues and may contribute to recovery after stroke. 1 Angiogenesis occurs in human brain after stroke, with endothelial cell proliferation after 3 to 4 days, a dense capillary network by 1 week, and neovascular infiltration by 2 to 4 weeks. 2 Within 3 months, microvessel density in the infarct area increases relative to the contralateral side, and extracts of infarcted brain tissue induce angiogenesis in chick chorioallantoic membranes. 3 These alterations may help to restore cerebral blood flow in stroke survivors 4 and protect against recurrent ischemia. Therefore, investigating mechanisms of angiogenesis after cerebral hypoxia or ischemia may provide new insights into stroke pathophysiology and treatment.Endoglin (CD105) is a homodimeric membrane protein that binds transforming growth factor (TGF)-␤1 and -␤3. 5 Loss-of-function mutations in the human gene ENG cause hereditary hemorrhagic telangiectasia (Osler-Rendu-Weber disease), 6 which produces capillary and venous telangiectases affecting the skin, mucous membranes, and respiratory, gastrointestinal, and urinary tracts. 7 Endoglin is upregulated in tumor vasculature, and the density of endoglinimmunopositive microvessels correlates inversely with cancer survival. 8,9 Endoglin is also overexpressed in endothelial cells of healing wounds, embryos, psoriatic skin, and rheumatoid synovia, 10 -12 suggesting that it is an endothelial proliferation marker. Vascular smooth muscle development and endothelial remodeling are defective in endoglinknockout mice. 7 Hypoxic regulation of gene expression involves extracellular signal-related kinase (ERK), which is widely associated with cell survival, and p38 mitogen-activated protein kinase (MAPK) and Jun amino-terminal kinase (JNK), whic...

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Borrelia BurgdorferiUpregulates the Adhesion Molecules E-selectin, P-selectin, ICAM-1 and VCAM-1 on Mouse Endothelioma Cellsin vitro

Cited by 51 publications

References 53 publications

Helicobacter pylori-Induced Activation of Human Endothelial Cells

Helicobacter pylori-Induced Activation of Human Endothelial Cells

Lyme Arthritis: Current Concepts and a Change in Paradigm

Hypoxic Induction of Endoglin via Mitogen-Activated Protein Kinases in Mouse Brain Microvascular Endothelial Cells

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