Angiotensin II induces CD62L shedding in human neutrophils
| العنوان: | Angiotensin II induces CD62L shedding in human neutrophils |
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| المؤلفون: | Inmaculada Ventura, Antonio Vega, Rajaa El Bekay, Javier Monteseirín, Pedro Chacón |
| المساهمون: | Junta de Andalucía |
| المصدر: | Digital.CSIC. Repositorio Institucional del CSIC instname |
| سنة النشر: | 2008 |
| مصطلحات موضوعية: | MAPK/ERK pathway, medicine.medical_specialty, Endothelium, Neutrophils, p38 mitogen-activated protein kinases, Down-Regulation, Small GTPases, Biology, Umbilical vein, Receptor, Angiotensin, Type 1, Phosphatidylinositol 3-Kinases, Internal medicine, medicine, Cell Adhesion, CD62L, Humans, L-Selectin, Protein kinase A, Mitogen-Activated Protein Kinase 1, Angiotensin II receptor type 1, Mitogen-Activated Protein Kinase 3, ERK1/2, Kinase, PI-3-kinase, Angiotensin II, Calcineurin, Cell biology, Endocrinology, medicine.anatomical_structure, Mitogen-Activated Protein Kinases, Cardiology and Cardiovascular Medicine |
| الوصف: | Studies indicate that both alterations in leukocyte and endothelial cell adhesion molecules and the renin angiotensin system are involved in the pathogenesis of atherosclerosis processes in human hypertension. The present work was undertaken to investigate whether angiotensin II (Ang II) regulates the expression of CD62L on human neutrophils. Human neutrophils were stimulated with Ang II in the presence of various AT1-receptor antagonists and protein kinase inhibitors, and CD62L cell surface expression was detected by flow cytometry. We report for the first time that Ang II down-regulated CD62L from the surface of human neutrophils, a process which was independent of neutrophil adhesion to endothelium since neutrophils were still able to adhere to human umbilical vein endothelial cells even under doses that almost completely release CD62L from the cell surface. This process occurred through pathways involving AT1 receptors, extracellular signal-regulated kinases 1 and 2 mitogen-activated protein kinase (MAPK), phosphatidylinositol 3-kinase, and calcineurin, ruling out a role for p38 MAPK and small GTPases in the process. © 2009 Elsevier Ireland Ltd. This work was funded by grants from the Consejería de Salud, Junta de Andalucía (SAS-55/04). J.M. is working within the Programa de Intensificación de la Actividad Investigadora en el Sistema Nacional de Salud. |
| تدمد: | 1879-1484 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::2e1a065204ab37f98ffa7dd90a0eae36Test https://pubmed.ncbi.nlm.nih.gov/19837408Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....2e1a065204ab37f98ffa7dd90a0eae36 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 18791484 |
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