Endothelial cell adhesion molecule and PMNL response to inflammatory stimuli and AGE-modified fibronectin

Sengoelge, Gürkan; Födinger, Manuela; Skoupy, Sonja; Ferrara, Ilse; Zangerle, Christa; Rogy, Michael A.; Hörl, Walter H.; Sunder‐Plassmann, Gere; Menzel, J

doi:10.1046/j.1523-1755.1998.00157.x

Cited by 54 publications

(39 citation statements)

References 38 publications

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“…The surface expression of P-selectin as an early and critical event in endothelial dysfunction is supported by previous reports of fast upregulation of endothelial cell P-selectin by ROS (16,18,47). Our results, with a short activation period, differ from previous findings; much longer incubation periods for cell adhesion molecules appearance (18 h) were reported for other mediators such as oxidized LDL or advanced glycation end products (11,40). This discrepancy can be explained by the different nature of the stimulants used.…”

Section: Discussionsupporting

confidence: 78%

Priming of polymorphonuclear leukocytes: a culprit in the initiation of endothelial cell injury

Jacobi¹,

Sela²,

Cohen³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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Peripheral polymorphonuclear leukocytes (PMNL) in hemodialysis (HD) patients are primed, continually releasing and exposing the vascular endothelium to soluble factors such as reactive oxygen species and inflammatory mediators. To mimic the close proximity between PMNL and the endothelial monolayer and to monitor and characterize the influence of soluble mediators released from PMNL, we developed a novel cocultivation system using primary human umbilical vein endothelial cell (HUVEC) cultures and PMNL, with a sieve separating the two cell types to prevent direct adhesive effects. PMNL (10 6 ) from HD patients or from healthy normal controls were cocultivated with HUVEC (10 5 ) for 15 min, and endothelial cell injury was assessed by HUVEC morphology, cell detachment, and apoptosis. Proinflammatory changes were estimated by expression of HUVEC adhesion molecule P-selectin and by endothelial IL-8 and endothelial nitric oxide synthase mRNA. The levels of intracellular tissue factor reflected the procoagulant state, whereas NADPH oxidase activity served as an indicator for prooxidative changes in HUVEC. Mediators released from the primed PMNL triggered activation/dysfunction of endothelial cells, causing 1) an increase in endothelial cell detachment and apoptosis, 2) a proinflammatory state manifested by increased IL-8 mRNA expression and P-selectin on the endothelial surface, 3) activation of endothelial NADPH oxidase, 4) an increase in endothelial cell tissue factor that directly correlated with PMNL priming index, and 5) a decrease in endothelial nitric oxide synthase mRNA. Our data support a pathogenic link between PMNL priming and endothelial dysfunction, suggesting that PMNL priming is a potential new nontraditional risk factor for the development of atherosclerosis. cocultivation; nicotinamide adenine dinucleotide phosphate oxidase; polymorphonuclear leukocyte priming index

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Section: Discussionsupporting

confidence: 78%

Priming of polymorphonuclear leukocytes: a culprit in the initiation of endothelial cell injury

Jacobi¹,

Sela²,

Cohen³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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“…3) AGEs enhance the expression of cell adhesion molecules, including ICAM-1 on vascular endothelial cells (27,28). 4) Shear stress could also stimulate the induction of ICAM-1 (29).…”

Section: Discussionmentioning

confidence: 99%

Intercellular Adhesion Molecule-1–Deficient Mice Are Resistant Against Renal Injury After Induction of Diabetes

et al. 2003

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“…It plays a major role in the maintenance of endothelial integrity. The risk factors which are involved in the pathogenesis of atherosclerosis such as advanced glycation end products (AGEs), LDL, oxidant stress with infectious complications and inflammatory stimuli (LPS, IL-1 and TNF-a) may increase PECAM-1 expression on endothelial cells 17,18 . Our results show that increased expression of ICAM-1 and PECAM-1 occurs when endothelial cells are stimulated with fetal plasma from pregnancies with umbilical placental vascular disease.…”

Section: Discussionmentioning

confidence: 99%

Endothelial cell expression of adhesion molecules is induced by fetal plasma from pregnancies with umbilical placental vascular disease

Wang¹

2002

BJOG: An International Journal of Obstetrics and Gynaecology

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Objective To test the hypothesis that local production with spill into the fetal circulation of factor(s) injurious to endothelium is responsible for the vascular pathology present when the umbilical artery Doppler study is abnormal. Expression of adhesion molecules is a feature of endothelial cell activation. Design Case -control study.Setting University teaching hospital.Samples Fetal plasma was collected from 27 normal pregnancies, 39 pregnancies with umbilical placental vascular disease defined by abnormal umbilical artery Doppler and 11 pregnancies with pre-eclampsia and normal umbilical artery Doppler. Methods Isolated and cultured human umbilical vein endothelial cells from normal pregnancies were incubated with fetal plasma from three study groups. mRNA expression of intercellular cell adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and platelet-endothelial cell adhesion molecule-1 (PECAM-1) were assessed by reverse transcription-polymerase chain reaction. To confirm the occurrence of this in vivo, we measured the levels of soluble fractions of sICAM-1, sVCAM-1 and sPECAM-1 in the fetal circulation in the fetal plasma used for endothelial cell incubation. Results The mRNA expression of ICAM-1 [median 1.1 (interquartile range 0.5-1.9) vs 0.7 (0.3 -1.2), P < 0.05] and PECAM-1 [2.1 (1.2 -3.0) vs 1.5 (0.7 -2.1), P < 0.05] was significantly higher following incubation with fetal plasma from umbilical placental vascular disease compared with the normal group. There was no difference in the expression of VCAM-1 [1.2 (0.9 -1.8) vs 1.1 (0.8 -1.6), ns]. The group with maternal preeclampsia and normal umbilical artery Doppler did not differ from the normal group. In the umbilical placental vascular disease group, the results were similar in the presence or absence of pre-eclampsia. For soluble fractions of the adhesion molecules released into the fetal circulation, we found the levels (ng/mL) of sICAM-1 [median 248.5 (interquartile range 197.3 -315.7) vs 174.2 (144.5 -212.9), P < 0.05] and sPECAM-1 [9.3 (6.2 -11

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Endothelial cell adhesion molecule and PMNL response to inflammatory stimuli and AGE-modified fibronectin

Cited by 54 publications

References 38 publications

Priming of polymorphonuclear leukocytes: a culprit in the initiation of endothelial cell injury

Priming of polymorphonuclear leukocytes: a culprit in the initiation of endothelial cell injury

Intercellular Adhesion Molecule-1–Deficient Mice Are Resistant Against Renal Injury After Induction of Diabetes

Endothelial cell expression of adhesion molecules is induced by fetal plasma from pregnancies with umbilical placental vascular disease

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