Activated neutrophil by endothelin-1 caused tissue damage in human umbilical cord

Halim, Abdul; Kanayama, Naohiro; Maradny, Emad Ei; Maehara, Kayoko; Terao, Toshihiko

doi:10.1016/0049-3848(95)93835-n

Cited by 40 publications

(30 citation statements)

References 18 publications

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“…This is in accordance with previous findings demonstrating that ETs up-regulate integrin expression in human neutrophils [9], promote neutrophil adhesion to human coronary artery endothelial cells [10] and activate neutrophils to cause damage to human umbilical cord [11].…”

Section: Discussionsupporting

confidence: 82%

“…Ishida et al, [8] showed that ET-1 primes neutrophils for an enhanced superoxide production by chemotactic peptides. The ETs were also shown to up-regulate the expression of CD11b/CD18 in human neutrophils [9], to promote neutrophil adhesion to human coronary artery endothelial cells [10] and to activate neutrophils to cause damage to human umbilical cord [11]. The biological effects of ETs in human neutrophils are believed to be mediated mainly via the ET A receptor subtype which they predominantly express [10].…”

Section: Introductionmentioning

confidence: 96%

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Endothelins Mediate Neutrophil Activation, ProMMP-9 Release and Endothelial Cell Detachment

et al. 2007

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Neutrophils isolated from human peripheral blood added to a monolayer of human endothelial cells (ECV-304 cell line) stimulated with LPS (100 ng ml(-1)) resulted in: (a) neutrophil activation, measured by spreading and release of leukotriene B(4) (LTB(4)); (b) neutrophil degranulation, measured by release of matrix pro-metalloproteinase-9 (proMMP-9) and (c) loss of the monolayer integrity due to detachment of the endothelial cells. Stimulation of endothelial cells with tumor necrosis factor-alpha (TNF-alpha 10 ng ml(-1)) or interleukin-1 (IL-1; 10 ng ml(-1)) induced a similar dose-dependent increase in the neutrophil activation and endothelial cell detachment. Pre-treatment of LPS-activated ECV-304 cells with [Phe22]BigET-1(19-37) (10(-9) M; an inhibitor of endothelin converting enzyme (ECE)) or addition of BQ-123 (10(-6) M; a selective endothelin A (ET(A)) receptor antagonist) to the co-cultures, significantly reduced neutrophil spreading (50-70% inhibition) as well as the levels of LTB(4) (70-100% inhibition) and proMMP-9 (40-50% inhibition) in the co-culture supernatants. In addition, the detachment of endothelial cells was also reduced (60-75% inhibition). Moreover, the exogenous addition of ET-1 (10(-9) M) to neutrophil suspensions induced neutrophil spreading and release of LTB(4) and proMMP-9. Taken together, these findings indicate that neutrophils added to stimulated endothelial cells in the co-culture system employed in this study, get activated by products of these cells and degranulate. In parallel, the detachment of endothelial cell monolayer from the culture plates, possibly by the action of neutrophil granule-derived gelatinases, is observed. Endothelins (ETs) produced by the endothelial cells are suggested to play an essential role in these phenomena.

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Section: Discussionsupporting

confidence: 82%

Section: Introductionmentioning

confidence: 96%

Endothelins Mediate Neutrophil Activation, ProMMP-9 Release and Endothelial Cell Detachment

et al. 2007

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“…For example, ET-1 may activate neutrophils to release increased quantities of granule contents (27). ET-1 has been also shown to stimulate endothelial cells, mast cells and macrophages (28)(29)(30)(31). Since treatment of bosentan was associated with increased numbers of broken nests and lower numbers of intact nests, we may suggest that ET-1 played a direct role in the ability of host macrophages to deal with the infection.…”

Section: Discussionmentioning

confidence: 99%

Endothelin-1 receptors play a minor role in the protection against acute Trypanosoma cruzi infection in mice

Roffê

Souza

Machado

et al. 2007

Braz J Med Biol Res

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Chagas' disease, caused by the protozoan Trypanosoma cruzi, is a major cause of cardiovascular disability in countries where it is endemic. Damage to the heart microvasculature has been proposed to be an important factor in the pathogenesis of heart dysfunction. Endothelin-1 (ET-1) is a potent vasoconstrictor and exerts its effects via specific ET A and ET B receptors. A few studies have suggested a role for ET-1 and its receptors in the pathogenesis of Chagas' disease. We investigated the effects of treatment with bosentan, an ET A /ET B receptor antagonist, on the course of T. cruzi infection (Y strain) in C57Bl/6 mice. Treatment with bosentan (100 mg kg -1 day -1 ) was given per os starting day 0 after infection until sacrifice. Bosentan significantly increased myocardial inflammation, with no effects on parasitemia. Although the total number of nests was similar, a lower number of intact amastigote nests was found in the heart of bosentan-treated animals. Bosentan failed to affect the infection-associated increase in the cardiac levels of the cytokines IFN-γ and TNF-α and the chemokines CCL2/MCP-1, CCL3/MIP-1α and CCL5/RANTES. In vitro, pre-incubation with ET-1 (0.1 µM) 4 h before infection enhanced the uptake of the parasites by peritoneal macrophages, and this effect was abrogated when macrophages were pre-treated with bosentan (1 µM) 15 min before incubation with ET-1. However, ET-1 did not alter killing of intracellular parasites after 48 h of in vitro infection. Our data suggest that bosentan-treated mice have a delay in controlling parasitism which is compensated for exacerbated inflammation. Infection is eventually controlled in these animals and lethality is unchanged, demonstrating that ET-1 plays a minor role in the protection against acute murine T. cruzi infection.

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“…ET-l, the most abundant of the ET peptides in the cardiovascular system, is the most potent endogenous vasoconstrictor (26,27). It is also important modulator of neutrophil function and a stimulator of adhesion molecules (28,29). While increasing microvascular vasoconstriction and leukocytes adhesiveness to microvessel, ET-1 might aggravate noreflow.…”

Section: Discussionmentioning

confidence: 99%

Relationship between no-reflow phenomenon and serotonin levels in patients with acute ST-elevation myocardial infarction who underwent primary percutaneous intervention

Topsakal¹,

Kaya²,

Karakaya³

et al. 2010

Anadolu Kardiyol Derg

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Objective: Our aim was to investigate the effects of serotonin, which is a severe vasoconstrictor agent, on the occurrence of no-reflow phenomenon. Methods: In this cross-sectional controlled study, 40 patients, admitted to our clinic with chest pain in the first 12 hours and underwent primary percutaneous coronary intervention because of acute myocardial infarction were enrolled. Patients with TIMI 0 grade basal flow and normal post-procedure flow were included in group 1 and patients with flow grade TIMI ≤were enrolled in group 2. To measure the serotonin levels, blood samples were collected from the coronary ostium before the procedure. Results: In group 1, there were 25 patients (20 males, 5 females) and the mean age was 58±11 years; in group 2 there were 15 patients (13 males, 2 females) and the mean age was 62±8 years. The mean serotonin level in platelet in group 1 was 476±208 ng/10 9 platelet and in group 2-542±273 ng/10 9 platelet. The difference was not statistically significant (p=0.39). When we compared the serum serotonin levels, it was 41.4±40.8 ng/ml for group 1, but 66.7±45.7 ng/ml for group 2. Although the serum serotonin levels were higher in group 2, the difference was not statistically significant (p=0.07). Conclusion: There was no effect of serotonin level in the development of no-reflow, in patients to whom primary coronary percutaneous intervention was applied. (Anadolu Kardiyol Derg 2010; 10: 253-9) Key words: No-reflow phenomenon, serotonin, vasoconstriction, myocardial infarction ÖZET Amaç: Çalışmamızın amacı, vazokonstriktör bir ajan olan serotoninin no-reflow fenomeni gelişimi üzerine olan etkisini araştırmaktı. Yöntemler: Bu enine-kesitli kontrollü çalışmaya akut miyokart enfarktüsü nedeniyle, göğüs ağrılarının ilk 12 saati içinde kliniğimize başvuran ve primer perkütan girişim uygulanan 40 hasta alındı. İşlem öncesi akım TIMI 0 iken işlem sonrası akım normal olanlar grup 1'i, işlem sonrası akım TIMI ≤2 olanlar grup 2'yi oluşturdu. Serotonin düzeyini ölçmek için işlem öncesi koroner ostiumdan kan alındı. Bulgular: Grup 1'de 25 hasta (20 erkek, 5 kadın) vardı, ortalama yaş 58±11 yıl idi; Grup 2' de 15 hasta vardı (13 erkek, 2 kadın) ve ortalama yaş 62±8 yıl idi. Grup'1 de trombosit içi ortalama serotonin düzeyi 476±208 ng/10 9 trombosit ve grup 2'de 542±273 ng/10 9 trombosit idi. Fark istatistiksel olarak anlamlı değildi (p=0.39). Serum serotonin düzeyi grup'1 de 41.4±40.8 ng/ml, grup'2 de 66.7±45.7 ng/ml olarak bulundu. Aradaki fark anlamlı değildi (p=0.07). Relationship between no-reflow phenomenon and serotonin levels in patients with acute ST-elevation myocardial infarction who underwent primary percutaneous intervention Akut ST yükselmeli miyokart enfarktüsü nedeniyle primer perkütan girişim uygulanan hastalarda no-reflow fenomeni ile serotonin düzeyi arasındaki ilişki

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Activated neutrophil by endothelin-1 caused tissue damage in human umbilical cord

Cited by 40 publications

References 18 publications

Endothelins Mediate Neutrophil Activation, ProMMP-9 Release and Endothelial Cell Detachment

Endothelins Mediate Neutrophil Activation, ProMMP-9 Release and Endothelial Cell Detachment

Endothelin-1 receptors play a minor role in the protection against acute Trypanosoma cruzi infection in mice

Relationship between no-reflow phenomenon and serotonin levels in patients with acute ST-elevation myocardial infarction who underwent primary percutaneous intervention

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