Age-related change in the retinoid X receptor beta gene expression in peripheral blood mononuclear cells of healthy volunteers: Effect of 13- cis retinoic acid supplementation

The regulation of cell growth and differentiation and also expression of a number of genes by retinoids are mediated by nuclear retinoid receptors (RARs and/or RXRs). In this study we investigated age-related alteration in both RAR and RXR receptor subtypes gene expression and tissue transglutaminas...

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Veröffentlicht in:Mechanisms of ageing and development 2007-11, Vol.128 (11), p.594-600
Hauptverfasser: Brtko, J., Rock, E., Nezbedova, P., Krizanova, O., Dvorcakova, M., Minet-Quinard, R., Farges, M.-C., Ribalta, J., Winklhofer-Roob, B.M., Vasson, M.-P., Macejova, D.
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Sprache:eng
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Zusammenfassung:The regulation of cell growth and differentiation and also expression of a number of genes by retinoids are mediated by nuclear retinoid receptors (RARs and/or RXRs). In this study we investigated age-related alteration in both RAR and RXR receptor subtypes gene expression and tissue transglutaminase (tTG) activity before and after supplementation with 13- cis retinoic acid (13cRA) in human peripheral blood mononuclear cells (PBMCs). Healthy men (40) were divided in two groups according to their age (young group: 26.1 ± 4.1 years and old group: 65.4 ± 3.8 years). Each volunteer received 13cRA (Curacné ®, 0.5 mg/(kg day)) during a period of 4 weeks. We have shown that RXRβ expression was decreased significantly ( p = 0.0108) in PBMCs of elderly men when compared to that of young volunteers. Distribution of retinoic acid receptor subtype expression in PBMCs was found in the order: RXRβ > RARγ > RXRα > RARα. The tTG activity in PBMCs reflected a trend to be enhanced after 13- cis retinoic acid supplementation. In conclusion, we demonstrate a significant decrease in the expression of RXRβ subtype of rexinoid receptors in PBMCs of healthy elderly men. Our data suggest that in healthy elderly men reduction of RXRβ expression in PBMCs might be a common feature of physiological senescence.
ISSN:0047-6374
1872-6216
DOI:10.1016/j.mad.2007.08.005