Up-regulation of steroid sulphatase activity in HL60 promyelocytic cells by retinoids and 1α,25-dihydroxyvitamin D3

Abstract

HL60 promyeloid cells express both classes of oestrogen receptor (ERalpha and ERbeta). We show that hydrolysis of oestrone sulphate by steroid sulphatase is a major source of oestrone in HL60 cells, and that most of the released oestrone is not metabolized further to 17beta-oestradiol. Treatment of HL60 cells with retinoids or 1alpha,25-dihydroxyvitamin D3 increased steroid sulphatase mRNA and activity in parallel with the induction of CD11b, an early marker of myeloid differentiation that is expressed before the differentiating cells stop proliferating. Use of agonists and antagonists against retinoid receptor-alpha and retinoid receptor-X revealed that both classes of retinoid receptor can drive steroid sulphatase up-regulation. Steroid sulphatase activity fluctuates during the cell cycle, being highest around the transition from G1 to S phase. During the differentiation of HL60 cells induced by all-trans-retinoic acid or 1alpha,25-dihydroxyvitamin D3, there is increased conversion of 17beta-oestradiol into oestrone by an oxidative 17beta-hydroxysteroid dehydrogenase. Treatment of Caco-2 colon adenocarcinoma cells with all-trans-retinoic acid or 1alpha,25-dihydroxyvitamin D3 also increases 17beta-oestradiol oxidation to oestrone. An increase in local oestrone production therefore occurs in multiple cell types following treatment with retinoids and 1alpha,25-dihydroxyvitamin D3. The possible involvement of locally produced oestrogenic steroids in regulating the proliferation and differentiation of myeloid cells is discussed.

Phosphorylation of Histone H3 Thr-45 Is Linked to Apoptosis

“…Thus, H3T45ph is induced in HL60 cells following the addition of DMSO to the cells. A DMSO-induced increase in cd11b mRNA, a granulocytic marker (18), confirms that the HL60 cells were differentiating (Fig. 2B).…”

Expression of WASP and Scar1/WAVE1 actin‐associated proteins is differentially modulated during differentiation of HL‐60 cells

“…For our cells, VD 3 treatment resulted in a non-adherent differentiated phenotype with induction in CD11b expression (Table I) and in the capacity to reduce NBT (not shown) [Hughes et al, 2001]. Scar1 expression was down-regulated but only to the extent observed for non-adherent monocytes/ macrophages obtained from petri dish cultures treated with PMA (Fig.…”

“…However, Scar1 expression was not modified in the ATRA-resistant cell lines K562 and HL-60 RES variant. In addition to their granulocytic differentiation potential, vitamin D 3 (VD 3 ) or phorbol 12-myristate 13-acetate (PMA) treatments induce a monocyte/macrophage-like phenotype in HL-60 cells [Hughes et al, 2001;Macfarlane and Manzel, 1994]. Differentiation to monocytes/macrophages resulted in the decrease of both Scar1 and WASP expression, even in the presence of monocytic differentiation inhibitor, the glucocorticoid dexamethasone [Nockher and Scherberich, 1997].…”

Egg–laying capacity is limited by carotenoid pigment availability in wild gulls Larus fuscus

“…One possible explanation is that supplemental carotenoids increased the synthesis and/or antioxidant protection of yolk precursors. Carotenoids and retinoic acid (a vitamin A metabolite, ultimately derived from pro-vitamin A carotenoids such as β-carotene) stimulate expression of oestrogenic enzymes, which have been shown to increase oestrogen production in vitro (Ng et al 2000;Hughes et al 2001). Oestrogen stimulates hepatic expression of the genes that code for synthesis of very low-density lipoprotein (VLDL) and vitellogenin, the main sources of yolk lipid and protein, respectively (Speake et al 1998).…”