Enhanced Expression of Cell Adhesion Molecules in the Aorta of Diabetic Mice is Mediated by gp91phox-derived Superoxide
The Korean Journal of Physiology and Pharmacology
;
: 109-115, 2005.
Artículo
en Inglés
| WPRIM
| ID: wpr-727662
ABSTRACT
Endothelial activation and subsequent recruitment of inflammatory cells are important steps in atherogenesis. The increased levels of cell adhesion molecules (CAM) have been identified in diabetic vasculatures, but the underlying mechanisms remain unclear. To determine the relationship among vascular production of superoxide, expression of CAM and diabetes, superoxide generation and expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), E- and P-selectin in the aorta from control (C57BL/6J) and diabetic mice (ob/ob) were measured. In situ staining for superoxide using dihydroethidium showed an increased superoxide production in diabetic aorta, accompanied with an enhanced NAD (P) H oxidase activity. Immunohistochemical analysis revealed that the endothelial expression of ICAM-1 (3.5+/-0.4) and VCAM-1 (3.8+/-0.3) in diabetic aorta was significantly higher than those in control aorta (0.9+/-0.5 and 1.6+/-0.3, respectively), accompanied with the enhanced expression of gp91phox, a membrane subunit of NAD (P) H oixdase. Furthermore, there was a strong positive correlation (r=0.89, P< 0.01 in ICAM-1 and r=0.88, P< 0.01 in VCAM-1) between ICAM-1/VCAM-1 expression and vascular production of superoxide. The present data indicate that the increased production of superoxide via NAD (P) H oxidase may explain the enhanced expression of CAM in diabetic vasculatures.
Texto completo:
Disponible
Índice:
WPRIM (Pacífico Occidental)
Asunto principal:
Aorta
/
Oxidorreductasas
/
Moléculas de Adhesión Celular
/
Adhesión Celular
/
Superóxidos
/
Molécula 1 de Adhesión Intercelular
/
Molécula 1 de Adhesión Celular Vascular
/
Selectina-P
/
Selectina E
/
Aterosclerosis
Límite:
Animales
Idioma:
Inglés
Revista:
The Korean Journal of Physiology and Pharmacology
Año:
2005
Tipo del documento:
Artículo
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