Effect of endothelin-1 on neutrophil adhesion to endothelial cells and perfused heart.

Farré, Antonio López; Riesco, Amparo; Espinosa, Gaudêncio; Digiuni, Enzo; Cernadas, M R; Álvarez, Vicente; Montón, Mercedes; Rivas, F; Gallego, M J; Egido, Jesús

doi:10.1161/01.cir.88.3.1166

Cited by 190 publications

(140 citation statements)

References 24 publications

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“…Among the proteins regulating the inflammatory response to cardiac ischemia, endothelin-1 (ET-1) plays an important role. Indeed ET-1 is involved in neutrophil trafficking and increases cardiac microvascular permeability (4,5). After the edema step, the healing process proceeds to the formation of granulation tissue, which is characterized by the presence of fibroblasts, macrophages, myofibroblasts, new blood vessels, and extracellular matrix proteins (6,7), ultimately resulting in scar formation, which is characterized by acellular and cross-linked collagen-rich regions (8)(9)(10)(11).…”

mentioning

confidence: 99%

Loss of Mouse P2Y4 Nucleotide Receptor Protects against Myocardial Infarction through Endothelin-1 Downregulation

Horckmans

Esfahani

Beauloye

et al. 2015

The Journal of Immunology

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Nucleotides are released in the heart under pathological conditions, but little is known about their contribution to cardiac inflammation. The present study defines the P2Y4 nucleotide receptor, expressed on cardiac microvascular endothelial cells and involved in postnatal heart development, as an important regulator of the inflammatory response to cardiac ischemia. P2Y4-null mice displayed smaller infarcts in the left descending artery ligation model, as well as reduced neutrophil infiltration and fibrosis. Gene profiling identified inter alia endothelin-1 (ET-1) as one of the target genes of P2Y4 in ischemic heart. The reduced level of ET-1 was correlated with reduction of microvascular hyperpermeability, neutrophil infiltration, and endothelial adhesion molecule expression, and it could be explained by the decreased number of endothelial cells in P2Y4-null mice. Expression analysis of metalloproteinases and their tissue inhibitors in ischemic heart revealed reduced expression of matrix metalloproteinase (MMP)-9, reported to be potentially regulated by ET-1, and MMP-8, considered as neutrophil collagenase, as well as reduction of tissue inhibitor of MMP-1 and tissue inhibitor of MMP-4 in P2Y4-null mice. Reduction of cardiac permeability and neutrophil infiltration was also observed in P2Y4-null mice in LPS-induced inflammation model. Protection against infarction resulting from loss of P2Y4 brings new therapeutic perspectives for cardiac ischemia and remodeling.

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mentioning

confidence: 99%

Loss of Mouse P2Y4 Nucleotide Receptor Protects against Myocardial Infarction through Endothelin-1 Downregulation

Horckmans

Esfahani

Beauloye

et al. 2015

The Journal of Immunology

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“…Migration of neutrophils from the intravascular compartment to an inflammed tissue requires interaction of neutrophils with vascular endothelium and the presence of chemoattractants which serve as homing triggers. ET-1 upregulates the expression of adhesive molecules, CD18 and CD11b on neutrophil surface, and enhances neutrophil adhesion to pulmonary endothelium [9,11,17]. The findings of an elevated serum ET-1 in P. aeruginosa-infected patients, but not the other pro-inflammatory cytokines, suggests an important role for ET-1 in the endothelial recruitment of neutrophils in bronchiectasis.…”

Section: Discussionmentioning

confidence: 99%

Endothelin-1 in stable bronchiectasis

Zheng¹,

Tipoe²,

Lam³

et al. 2000

Eur Respir J

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Endothelin (ET)-1 has been suggested to promote neutrophil adhesion to endothelium, migration to inflamed areas, and release of elastase. ET-1 might therefore play a role in the pathogenesis of bronchiectasis, a chronic inflammatory and infective airway disease which is still poorly understood.Thirty five patients with stable bronchiectasis (20 females, mean age SD 49.1 15.0 yrs) and 18 control subjects (8 females, 49.4 11.3 yrs) were recruited prospectively. The ET-1 levels in serum and sputum were measured by commercially available enzyme linked immunosorbent assay (ELISA) kits.Patients with Pseudomonas aeruginosa in their sputum had a significantly higher serum level of ET-1 (median 25.8, interquartile range 13±43.9 pg . mL -1 ) than patients without P. aeruginosa (0, 0±10.5 pg . mL -1 ; p=0.0004) and healthy control subjects (4.6, 0±16.3 pg . mL -1 ; p=0.002). However, patients with and without P. aeruginosa infection had no significant difference in sputum ET-1 level (p=0.15). There was no correlation between serum or sputum ET-1 levels with the serum and sputum levels of the interleukin (IL)-1b, IL-8 and tumour necrosis factor (TNF)-a; the number of bronchiectasis lung lobes; and spirometry. Serum ET-1 level correlated with 24 h sputum volume for the bronchiectasis patients (r=0.51, p=0.002).The results, therefore, suggest a significant pathogenic role for endothelin-1 among Pseudomonas aeruginosa-infected patients with bronchiectasis. Further studies should be performed to evaluate the clinico-pathological correlation and expression of endothelin-1 in bronchiectasis.

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“…On the other hand, PMNs increase the induction of ET-1 mRNA expression in endothelial cells (36) and convert big ET to ET-1 (37). Furthermore, ET-1 stimulates the expression of adhesive molecules, CD11/CD18 integrin, on the neutrophil surface (38). The expression of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 on cerebromicrovascular endothelial cell lines is also up-regulated by ET-1 (39).…”

Section: Discussionmentioning

confidence: 99%

Attenuation of Ischemic Liver Injury by Monoclonal Anti-Endothelin Antibody, AwETN40

Urakami

Todo

Zhu

et al. 1997

Journal of the American College of Surgeons

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Background-Enhanced production of endothelin-1 (ET-1), vasoconstrictive 21 amino acids produced by endothelial cells during ischemia and after reperfusion of the liver, is known to cause sinusoidal constriction and microcirculatory disturbances, which lead to severe tissue damage. Using a 2-hour hepatic vascular exclusion model in dogs, we tested our hypothesis that neutralization of ET-1 by monoclonal anti-ET-1 and anti-ET-2 antibody (AwETN40) abates vascular dysfunction and ameliorates ischemia/reperfusion injury of the liver.

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Effect of endothelin-1 on neutrophil adhesion to endothelial cells and perfused heart.

Cited by 190 publications

References 24 publications

Loss of Mouse P2Y4 Nucleotide Receptor Protects against Myocardial Infarction through Endothelin-1 Downregulation

Loss of Mouse P2Y4 Nucleotide Receptor Protects against Myocardial Infarction through Endothelin-1 Downregulation

Endothelin-1 in stable bronchiectasis

Attenuation of Ischemic Liver Injury by Monoclonal Anti-Endothelin Antibody, AwETN40

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