RETRACTED: ICAM-1 promotes the abnormal endothelial cell phenotype in chronic thromboembolic pulmonary hypertension
| العنوان: | RETRACTED: ICAM-1 promotes the abnormal endothelial cell phenotype in chronic thromboembolic pulmonary hypertension |
|---|---|
| المؤلفون: | Myriam Amsallem, Francois Haddad, Florence Lecerf, Jennifer Arthur Ataam, Olaf Mercier, Joanna Arthur Ataam, Stephanie Arthur Ataam, Saadia Eddahibi, Lilia Lamrani, Véronique Capuano, Maria Rosa Ghigna, Elie Fadel, Julien Guihaire |
| المصدر: | The Journal of Heart and Lung Transplantation. 38:982-996 |
| بيانات النشر: | Elsevier BV, 2019. |
| سنة النشر: | 2019 |
| مصطلحات موضوعية: | Male, Pulmonary and Respiratory Medicine, Pathology, medicine.medical_specialty, Hypertension, Pulmonary, medicine.medical_treatment, 030204 cardiovascular system & hematology, Metastasis, Pathogenesis, 03 medical and health sciences, 0302 clinical medicine, medicine.artery, medicine, Humans, Endothelial dysfunction, Cells, Cultured, Aged, Endarterectomy, Transplantation, ICAM-1, Cell adhesion molecule, business.industry, Endothelial Cells, Cancer, Middle Aged, Intercellular Adhesion Molecule-1, medicine.disease, 3. Good health, Phenotype, 030228 respiratory system, Chronic Disease, Pulmonary artery, Female, Surgery, Pulmonary Embolism, Cardiology and Cardiovascular Medicine, business |
| الوصف: | 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.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.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 (p0.001). 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.ICAM-1 contributes to maintaining the abnormal endothelial cell phenotype in CTEPH. |
| تدمد: | 1053-2498 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::a5463aba7e676d9c1747109388eae6b1Test https://doi.org/10.1016/j.healun.2019.06.010Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....a5463aba7e676d9c1747109388eae6b1 |
| قاعدة البيانات: | OpenAIRE |
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