Cardiff University | Prifysgol Caerdydd ORCA
Online Research @ Cardiff 
WelshClear Cookie - decide language by browser settings

Angiotensin II induces CD62L shedding in human neutrophils

Vega, Antonio, El Bekay, Rajaa, Chacon Fernandez, Pedro, Ventura, Inmaculada and Monteseirín, Javier 2010. Angiotensin II induces CD62L shedding in human neutrophils. Atherosclerosis 209 (2) , pp. 344-351. 10.1016/j.atherosclerosis.2009.09.067

Full text not available from this repository.


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.

Item Type: Article
Date Type: Publication
Status: Published
Schools: Biosciences
Publisher: Elsevier
ISSN: 0021-9150
Last Modified: 28 Jun 2019 02:02

Citation Data

Cited 7 times in Scopus. View in Scopus. Powered By Scopus® Data

Actions (repository staff only)

Edit Item Edit Item