被撤回的出版物: ICAM-1 promotes the abnormal endothelial cell phenotype in chronic thromboembolic pulmonary hypertension (Retracted article. See vol. 40, 2021)

JOURNAL OF HEART AND LUNG TRANSPLANTATION

卷:38

Article; Retracted Publication

Ataam, Jennifer Arthur^1,4  Mercier, Olaf^1,2  Lamrani, Lilia¹  Amsallem, Myriam^1,4  Ataam, Joanna Arthur⁵  Ataam, Stephanie Arthur¹  Guihaire, Julien^1,2  Lecerf, Florence¹  Capuano, Veronique¹  Ghigna, Maria Rosa^1,3  Haddad, Francois⁴  Fadel, Elie^1,2  Eddahibi, Saadia⁵ 

[1] Marie Lannelongue Hosp, Res & Innovat Unit, 133 Ave Resistance, F-92350 Le Plessis Robinson, France

[2] Marie Lannelongue Hosp, Dept Thorac & Vasc Surg & Heart Lung Transplantat, Le Plessis Robinson, France

[3] Marie Lannelongue Hosp, Dept Pathol, Le Plessis Robinson, France

[4] Stanford Univ, Dept Med, Stanford, CA 94305 USA

[5] Univ Montpellier, Montpellier, France

关键词: Chronic thromboembolic hypertension;    Endothelial dysfunction;    ICAM-1;    Adhesion molecules;    Survival signalling pathway;   

DOI  :  10.1016/j.healun.2019.06.010

来源: Elsevier

【 摘 要 】

BACKGROUND: Pulmonary endothelial cells play a key role in the pathogenesis of Chronic Thromboembolic Pulmonary Hypertension (CTEPH). Increased synthesis and/or the release of intercellular adhesion molecule-1 (ICAM-1) by pulmonary endothelial cells of patients with CTEPH has been recently reported, suggesting a potential role for ICAM-1 in CTEPH. METHODS: We studied pulmonary endarterectomy specimens from 172 patients with CTEPH and pulmonary artery specimens from 97 controls undergoing lobectomy for low-stage cancer without metastasis. RESULTS: ICAM-1 was overexpressed in vitro in isolated and cultured endothelial cells from endarterectomy specimens. Endothelial cell growth and apoptosis resistance were significantly higher in CTEPH specimens than in the controls (p < 0.001). Both abnormalities were abolished by pharmacological inhibition of ICAM-1 synthesis or activity. The overexpression of ICAM-1 contributed to the acquisition and maintenance of abnormal EC growth and apoptosis resistance via the phosphorylation of SRC, p38 and ERK1/2 and the overproduction of survivin. Regarding the ICAM-1 E469K polymorphism, the KE heterozygote genotype was significantly more frequent in CTEPH than in the controls, but it was not associated with disease severity among patients with CTEPH. CONCLUSIONS: ICAM-1 contributes to maintaining the abnormal endothelial cell phenotype in CTEPH. (C) 2019 International Society for Heart and Lung Transplantation. All rights reserved.

【 授权许可】

Free