Depósito Académico >
CIMA (Centro de Investigación Médica Aplicada) >
Área de Ciencias Cardiovasculares >
Cardiopatía hipertensiva >
DA - CIMA - Cardiovasculares - Cardiopatía hipertensiva - Artículos de Revista >
|The proinflammatory mediator CD40 ligand is increased in the metabolic syndrome and modulated by adiponectin|
|Authors: ||Natal, C. (Cristina)|
Restituto, P. (Patricia)
Iñigo, C. (Carmen)
Colina, I. (Inmaculada)
Diez, J. (Javier)
Varo, N. (Nerea)
|Keywords: ||CD40 Ligand/genetics|
Metabolic Syndrome X/genetics
|Issue Date: ||2008|
|Publisher: ||Endocrine Society|
|Publisher version: ||http://jcem.endojournals.org/content/93/6/2319|
|Citation: ||Natal C, Restituto P, Inigo C, Colina I, Diez J, Varo N. The proinflammatory mediator CD40 ligand is increased in the metabolic syndrome and modulated by adiponectin. J Clin Endocrinol Metab 2008 Jun;93(6):2319-2327.|
|OBJECTIVES: We hypothesized that the CD40/CD40 ligand (CD40L) system is up-regulated in the metabolic syndrome (MS) and modulated by adiponectin (AN). The objectives were: 1) to compare plasma and monocyte CD40L in patients with MS and controls and its association with clinical and biochemical parameters, 2) to investigate platelets as a source of soluble CD40L (sCD40L), and 3) to analyze the effects of AN on CD40/CD40L.
METHODS: Plasma sCD40L and AN were measured in 246 controls and 128 patients with MS by ELISA. Monocyte CD40/CD40L expression and platelet CD40L content and release were compared in patients with MS and controls. Monocytes and endothelial cells were cultured with AN and CD40/CD40L expression determined by real-time RT-PCR and Western blotting.
RESULTS: Patients with MS had higher sCD40L and lower AN levels than controls (0.89 +/- 0.1 vs. 0.76 +/- 0.07 ng/ml and 10.10 +/- 0.65 vs. 12.99 +/- 0.80 microg /ml, P < 0.05). Monocyte CD40/CD40L expression was higher (P < 0.05) in patients than controls (CD40: 1.31 +/- 0.31 vs. 0.80 +/- 0.14 arbitrary units; CD40L: 1.24 +/- 0.85 vs. 0.43 +/- 0.14 pg/microg protein). No differences were observed on CD40L content between resting platelets from patients with MS and controls (7.7 +/- 3.5 vs. 7.2 +/- 2.2 pg/microg protein). Stimulated platelets from patients with the MS released more (P < 0.05) sCD40L than controls (582 +/- 141 vs. 334 +/- 60% change vs. nonstimulated platelets). AN reduced CD40L mRNA and protein expression in monocytes from MS patients and endothelial cells.
CONCLUSIONS: The enhanced sCD40L and cellular CD40L expression in the MS suggests that CD40L is of pathophysiological relevance in MS. Also, a new antiinflammatory effect of AN is described through the modulation of the CD40/CD40L system.|
|Permanent link: ||http://hdl.handle.net/10171/21851|
|Appears in Collections:||DA - CIMA - Cardiovasculares - Cardiopatía hipertensiva - Artículos de Revista|
|Files in This Item:|
| View / Open |
Items in Dadun are protected by copyright, with all rights reserved, unless otherwise indicated.