Endothelial cell NADPH oxidase mediates the cerebral microvascular dysfunction in sickle cell transgenic mice Katherine C. Wood, Robert P. Hebbel * and D. Neil Granger 1 Department of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center, Shreveport, Louisiana, USA; and * Vascular Biology Center and Division of Hematology-Oncology-Transplantation, University of Minnesota Medical School, Minneapolis, Minnesota, USA 1 Correspondence: Department of Molecular and Cellular Physiology, LSU Health Sciences Center, 1501 Kings Hwy., Shreveport, LA 71130-3932, USA. E-mail: dgrang@lsuhsc.edu <h3>SPECIFIC AIMS</h3> Although blood cell-endothelial cell adhesion and oxidative stress have been implicated in the pathogenesis of sickle cell disease (SCD), the nature of the linkage between these vascular responses in SCD remains unclear. The objectives of this study were to determine whether reactive oxygen species (ROS) contribute to enhanced leukocyte and platelet adhesion responses in the microvasculature during SCD and to identify potential enzymatic and cellular sources of these ROS. <h3>PRINCIPAL FINDINGS</h3> 1. Reduced leukocyte and platelet adhesion in ß S /SOD-1TgN chimeric mice, with normal SOD expression by circulating ß S blood cells but overexpression of SOD in the vessel wall, strongly implicates endothelial cell-associated superoxide in these adhesion responses One objective of this study was to
/lp/fed-of-american-socs-for-experimental-biology/endothelial-cell-nadph-oxidase-mediates-the-cerebral-microvascular-07NM30gY0h