Microvascular endothelial cells from human omental tissue: Modified method for long-term cultivation and new aspects of characterization

Anders, E M; Alles, Jens Uwe; Delvos, U.; Pötzsch, Bernd; Preissner, Klaus T.; Müller‐Berghaus, Gert

doi:10.1016/0026-2862(87)90057-4

Cited by 42 publications

(20 citation statements)

References 25 publications

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“…The cytokeratin and ultrastructure results of the present studies support those of Visser et al [7] on the mésothélial origin of the covering layer of the omentum [9], The view of some authors [10][11][12] that these cells are of endothelial origin must finally be rejected. Our results on HOMES expression of vimentin and cytokeratins 8.…”

Section: Discussionsupporting

confidence: 80%

Effects of Cytokines on the Expression of Cell Adhesion Molecules by Cultured Human Omental Mesothelial Cells

et al. 1995

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Cultured mesothelial cells (HOMES) are very responsive to the proinflammatory cytokines, interleukin (IL)-l and tumor necrosis factor-α (TNF-α). E-selectin, ICAM-1 and VCAM-1 are known to play an important role, because they are presented by diverse cell types, for example endothelial cells (ECs), and interact with coresponding ligands on white blood cell membranes. In this study, the expression of ICAM-1, VCAM-1, E-selectin as well as PECAM-1 on cultured HOMES was studied over 5,24,48 and 72 h exposure to IL-1 β, interferon-γ and TNF-α. In previous studies we have shown that IL-l β and TNF-α increase the expression of ICAM-1, E-selectin and VCAM-1 on the cytoplasmatic membranes of HUVECs, HSVECs and HAFECs (ECs from human umbilical vein, saphenous vein and femoral artery, respectively). Using a comparative quantitative cell enzyme immunoassay, we found that expression of the adhesion molecules ICAM-1 and VCAM-1 was significantly increased on HOMES in a dose- and time-dependent manner, compared to nonstimulated cells. Thus, ICAM-1 increased dramatically after 5 h incubation with TNF-α. Values of about 450% of the control level were measured. VCAM-1 was similarly stimulated after 24 h incubation with the same cytokine, although its level of expression was significantly lower than that of ICAM-1. In contrast to findings in the literature, VCAM-1 was not found to be expressed constitutively. E-selectin was neither constitutively expressed nor markedly inducible on HOMES. Only weak expression was found after 24 h incubation with high-dose IL-lβ. PEC AM-1 was expressed constitutively, as became evident in antibody dilution studies. These data indicate that HOMES respond to inflammatory stimuli, in some ways in a similar fashion to vascular endothelial cells, but also show a specific pattern of antigen presentation. The results are important for a better understanding of inflammatory processes in serous cavities. The data are also relevant for the improvement of antithrombogenous surfaces of the lumina of vascular prostheses by cell seeding.

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Section: Discussionsupporting

confidence: 80%

Effects of Cytokines on the Expression of Cell Adhesion Molecules by Cultured Human Omental Mesothelial Cells

et al. 1995

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“…Confluent monolayers of cells passed only once into 24-well plates were used for experiments within 48-72 h after plating. Endothelial cells were identified by their morphology and by indirect immunofluorescence for Von Willebrand factor (9).…”

mentioning

confidence: 99%

α2-Macroglobulin Remains as Important as Antithrombin III for Thrombin Regulation in Cord Plasma in the Presence of Endothelial Cell Surfaces

Delorme

Berry³

et al. 1995

Pediatr Res

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---r =--9 ------------ __1 ----7 ---' ------71-7 -- ABSTRACTInfants and children rarely develop thrombotic complications compared with adults, suggesting that there are protective mechanisms in place for the young. Because endothelial cell surfaces regulate thrombin formation and inhibition, we compared thrombin regulation by human umbilical vein endothelial cell surfaces exposed to defibrinated cord and adult plasmas. After activation by either 10% activated partial thromboplastin reagent (strong activator) or coagulant phospholipids (weak activator) the following were measured: free thrombin, thrombin bound to antithrombin I11 (ATIII), heparin cofactor 11, a,-macroglobulin (a2M), and prothrombin concentration. Free thrombin activity was expressed as remaining activity, after subtraction of thrombin-a2M activity. After 10% activated partial thromboplastin reagent, 100% of prothrombin was consumed and significant amounts of thrombin generated by 2 min. Cord plasma generated significantly less thrombin than adult plasma, reflecting the lower initial plasma concentration of prothrombin. Correspondingly, concentrations of thrombin inhibitor complexes were significantly greater in adult plasma than in cord plasma. After coagulant phospholipids, 50% of prothrombin was consumed and negligible thrombin activity measured for both adult and cord plasma. Similar amounts of thrombin inhibitor complexes were formed. ATIII was the predominant inhibitor of thrombin in adult plasma, whereas a,M was as important as ATIII in cord plasma for both activators. When cord plasma concentrations of ATIII were increased to adult values, the proportion complexed to a2M decreased. We conclude that on human umbilical vein endothelial cells, the capacity to generate thrombin is decreased in adult and cord plasmas. Furthermore, a2M is at least as important an inhibitor as ATIII in cord plasma, even in the presence of Thromboembolic complications rarely occur in fetuses and newborns, suggesting that protective mechanisms are in place in the young. Biologically, the ability to regulate thrombin formation and activity are of central importance to the prevention and formation of large-vessel thrombi. Regulation of thrombin under physiologic circumstances involves both plasma coagulation and inhibitors, as well as interactions with

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“…When the endothelial cell layer is damaged, a hemostatic reaction starts on the exposed subendothelium and connective tissue. 12 Platelets will rapidly adhere to uncovered adhesive molecules, and coagulation will start due to the exposure of tissue factor. The components of the vessel wall involved in the initiation of the hemostatic response are synthesized predominantly by endothelial cells, smooth muscle cells (SMC), and fibroblasts (Fb).…”

mentioning

confidence: 99%

Thrombogenicity of vascular cells. Comparison between endothelial cells isolated from different sources and smooth muscle cells and fibroblasts.

Zwaginga¹,

Boer²,

Ijsseldijk³

et al. 1990

Arteriosclerosis

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When the endothelial cell layer Is damaged, a thrombotic reaction starts on the cells' subendothelium and on the connective tissue deposited by smooth muscle cells in the deeper layers. When more severe vascular damage occurs, hemostasis will Involve the vessel adventitia In which fibroblasts are found. In this article, the influence of in vitro cultured endothelial cells, smooth muscle cells, and fibroblasts on the hemostatic balance was studied. To do so, perfusions were performed with low molecular weight heparln antlcoagulated blood over the extracellular matrix of the cells. This method allowed the study of tissue factor-dependent thrombln generation and its influence on formation of fibrin and platelet aggregates. The experiments described in this article show that endothelial cells isolated from different human organs Interfere differently In the hemostatic response. Endothelial cells Isolated from umbilical veins are nonthrombogenic; they do not synthesize tissue factor under unstlmulated conditions. On their extracellular matrix, only adherent platelets are found, but no aggregates and no fibrin. Endothelial cells Isolated from omentum and atrium contain tissue factor activity under unstimulated conditions. As a consequence, thrombln Is generated on their surfaces, and platelet aggregates and fibrin deposition are found on the extracellular matrices after perfusions with whole blood. The matrix of smooth muscle cells and fibroblasts behaved similarly. Increase In shear rate and perfuslon time resulted In an Increase in platelet aggregate formation. Polymerized fibrin deposition decreased when perfusions were performed at higher shear. Both platelet aggregation and fibrin deposition were tissue factor dependent and could be blocked more than 70% by an antibody against tissue factor. Based on these results, we conclude that endothelial cells isolated from umbilical veins form the best nonthrombogenic surface In vitro. Moreover, coagulation-dependent hemostasis should be Included when thrombogenicity of subendothelium Is discussed, especially when it concerns matrix derived from cells present In the deeper layer of the vessel wall.

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Microvascular endothelial cells from human omental tissue: Modified method for long-term cultivation and new aspects of characterization

Cited by 42 publications

References 25 publications

Effects of Cytokines on the Expression of Cell Adhesion Molecules by Cultured Human Omental Mesothelial Cells

Effects of Cytokines on the Expression of Cell Adhesion Molecules by Cultured Human Omental Mesothelial Cells

α2-Macroglobulin Remains as Important as Antithrombin III for Thrombin Regulation in Cord Plasma in the Presence of Endothelial Cell Surfaces

Thrombogenicity of vascular cells. Comparison between endothelial cells isolated from different sources and smooth muscle cells and fibroblasts.

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