Annelienke van Hulst

15 General introduction 1 CORTICOSTEROID RECEPTORS AND GLUCOCORTICOID AFFINITY Glucocorticoids can bind and activate two receptor types: the glucocorticoid receptor (GR) and the mineralocorticoid receptor (MR). Both are members of the steroid receptor superfamily and are encoded by the NR3C1 and NR3C2 gene respectively. The GR and MR are structurally and functionally related. They are localized in the cytosol and upon ligand binding translocate into the nucleus, where they exert their actions through transcriptional activation or repression.12,13 The MR is expressed in numerous tissues: in epithelial tissues such as the kidney it is aldosterone selective and its main function is sodium and water retention, alongside potassium secretion.14 In other tissues such as heart, muscle, liver and brain, the MR is also present but its function is more complex.12 The GR is expressed in nearly all tissue types and is above all essential in maintaining physiological balance.13 Depending on the expressing tissue, the GR and MR show different affinities for cortisol which can lead to distinct effects.15,16 This effect is influenced by two key enzymes: 11betahydroxysteroid dehydrogenase (11β-HSD) 1 and 11β-HSD 2. 11β-HSD 2 metabolizes cortisol to inactive cortisone, therefore favoring binding of aldosterone to the MR. Conversely, 11β-HSD 1 converts cortisone to the active cortisol. The presence or absence of both enzymes in peripheral tissue mostly determines the effect of corticosteroids on both receptors. Glucocorticoids exert their cytotoxic effect on leukemic cells predominantly through activation of the GR. After binding of glucocorticoids to the GR, the complex is translocated to the nucleus where it can induce cell-cycle arrest and apoptosis through multiple pathways.17-20 Different synthetic glucocorticoids have different affinities for the GR and MR. Conventionally, dexamethasone is reported to be the most potent glucocorticoid with a sevenfold higher glucocorticoid activity than prednisolone, and no mineralocorticoid activity.5 Prednisolone exerts an effect through both receptors, although with higher affinity for the GR.5 However, these reports are based on anti-inflammatory and Na+- retaining potency. In pediatric ALL samples, previous studies showed that the in vitro anti-leukemic (cytotoxic) activity of dexamethasone is seventeen fold higher than prednisolone.21,22 However, different studies, using various models and evaluating diverse effects of glucocorticoids, show wide ranges of glucocorticoid and mineralocorticoid activity when comparing either dexamethasone, prednisolone or hydrocortisone.22-25 The anti-leukemic activity of these glucocorticoids and the role of the GR and MR in this cytotoxic effect therefore remains unclear.

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