Tumour-derived interleukin 1 alpha (IL-1 alpha) up-regulates the release of soluble intercellular adhesion molecule-1 (sICAM-1) by endothelial cells
| العنوان: | Tumour-derived interleukin 1 alpha (IL-1 alpha) up-regulates the release of soluble intercellular adhesion molecule-1 (sICAM-1) by endothelial cells |
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| المؤلفون: | Maresa Altomonte, Maria Rita Nicotra, Sandra Coral, Michele Maio, A Gasparollo, I. Cattarossi, P. G. Natali, Ester Fonsatti |
| المصدر: | Scopus-Elsevier British Journal of Cancer |
| سنة النشر: | 1997 |
| مصطلحات موضوعية: | Cancer Research, Endothelium, medicine.medical_treatment, Intercellular Adhesion Molecule-1, Umbilical vein, Immune system, Neoplasms, medicine, Humans, Cells, Cultured, biology, Interleukin, Molecular biology, Up-Regulation, Endothelial stem cell, medicine.anatomical_structure, Cytokine, Oncology, Urinary Bladder Neoplasms, Culture Media, Conditioned, Immunology, biology.protein, Endothelium, Vascular, Antibody, Interleukin-1, Research Article |
| الوصف: | Levels of circulating soluble intercellular adhesion molecule-1 (sICAM-1) are elevated in patients affected by solid malignancies; however, the cellular sources generating high levels of sICAM-1 remain to be characterized. Using conditioned media (CM) from seven ICAM-1-positive or -negative neoplastic cells, we demonstrate that tumour-derived interleukin 1alpha (IL-1alpha) significantly (P < 0.05) up-regulates the release of sICAM-1 by human umbilical vein endothelial cells. The intensity of the effect correlated with the amounts of IL-1alpha detectable in CM. Levels of ICAM-1 mRNA were also up-regulated by tumour-secreted IL-1alpha. The up-regulation of the shedding of sICAM-1 and of its expression at protein and mRNA level were completely reversed by the addition of anti-IL-1alpha neutralizing antibodies. Consistent with the in vitro data, tumour endothelia were strongly stained for ICAM-1 compared with autologous normal tissue endothelia. Taken altogether, our observations reveal an IL-1alpha-mediated tumour-endothelium relationship sustaining the shedding of sICAM-1 by endothelial cells. This is a general phenomenon in solid malignancies that correlates with the ability of neoplastic cells to secrete IL-1alpha rather than with their expression of ICAM-1 and/or histological origin. sICAM-1 has been previously shown to inhibit LFA-1/ICAM-1-mediated cell-cell interactions; therefore, the ability of neoplastic cells to secrete IL-1alpha is likely to represent a mechanism for their escape from immune interaction. Images Figure 5 Figure 6 |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::7572564e9aa1688d1c99d522aa22167d http://hdl.handle.net/11365/1081400 |
| حقوق: | OPEN |
| رقم الأكسشن: | edsair.doi.dedup.....7572564e9aa1688d1c99d522aa22167d |
| قاعدة البيانات: | OpenAIRE |
| الوصف غير متاح. |