The differentiating agent, retinoic acid, causes an early inhibition of inositol lipid-specific phospholipase C activity in HL-60 cells

Geny, Blandine; Cost, Hélène; Barreau, P.; Basset, M.; Peuch, Christian Le; Abita, Jean-Pierre; Cockcroft, Shamshad

doi:10.1016/0898-6568(91)90003-d

Cited by 19 publications

(3 citation statements)

References 34 publications

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“…In fact, ATRA has complex effects on PI‐PLC activity in HL60 cells. During the first 24–36 h following exposure to ATRA PI‐PLC activity appears to be inhibited and this is followed by an increase in nuclear PI‐PLC activity 48–72 h after exposure [Geny et al, 1991: Porfiri et al, 1991; Iirie et al, 1995; Ohoka et al, 1995; Lopez‐Pedrera et al, 2001].…”

Section: Discussionmentioning

confidence: 99%

Retinoid‐mediated stimulation of steroid sulfatase activity in myeloid leukemic cell lines requires RARα and RXR and involves the phosphoinositide 3‐kinase and ERK‐MAP kinase pathways

Hughes

Zhao

Chandraratna

et al. 2005

J of Cellular Biochemistry

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All-trans retinoic acid and 9-cis-retinoic acid stimulate the activity of steroid sulfatase in HL60 acute myeloid leukemia cells in a concentration- and time-dependent manner. Neither of these 'natural retinoids' augmented steroid sulfatase activity in a HL60 sub-line that expresses a dominant-negative retinoic acid receptor alpha (RARalpha). Experiments with synthetic RAR and RXR agonists and antagonists suggest that RARalpha/RXR heterodimers play a role in the retinoid-stimulated increase in steroid sulfatase activity. The retinoid-driven increase in steroid sulfatase activity was attenuated by inhibition of phospholipase D (PLD), but not by inhibitors of phospholipase C. Experiments with inhibitors of protein kinase C (PKC) show that PKCalpha and PKCdelta play an important role in modulating the retinoid-stimulation of steroid sulfatase activity in HL60 cells. Furthermore, we show that pharmacological inhibition of the RAF-1 and ERK MAP kinases blocked the retinoid-stimulated increase in steroid sulfatase activity in HL60 cells and, by contrast, inhibition of the p38-MAP kinase or JNK-MAP kinase had no effect. Pharmacological inhibitors of the phosphatidylinositol 3-kinase, Akt, and PDK-1 also abrogated the retinoid-stimulated increase in steroid sulfatase activity in HL60 cells. These results show that crosstalk between the retinoid-stimulated genomic and non-genomic pathways is necessary to increase steroid sulfatase activity in HL60 cells.

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Section: Discussionmentioning

confidence: 99%

Retinoid‐mediated stimulation of steroid sulfatase activity in myeloid leukemic cell lines requires RARα and RXR and involves the phosphoinositide 3‐kinase and ERK‐MAP kinase pathways

Hughes

Zhao

Chandraratna

et al. 2005

J of Cellular Biochemistry

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“…In keeping with this idea, the decrease in the expression of NIS protein has been observed after 24-36 h (Kogai et al 1997). However, this might not be the only action of these substances: within 1 h, retinoic acid modulates gap junction permeability in neurones and in numerous mammalian cells (Brummer et al 1991, Weiler et al 1999 and markedly reduces the concentrations of inositol phosphate and diacyl glycerol in HL-60 cells (Geny et al 1991).…”

Section: Introductionmentioning

confidence: 55%

Retinol has specific effects on binding of thyrotrophin to cultured porcine thyrocytes

Frőhlich¹,

Witke²,

Czarnocka³

et al. 2004

Journal of Endocrinology

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Retinoids are potential candidates for the treatment of thyroid cancer. However, one of the disadvantages of these substances is their dedifferentiating effect on normal non-transformed thyrocytes. To identify conditions under which no dedifferentiating effect of retinol on normal thyrocytes can be observed, we determined iodide uptake, protein iodination, expression of sodium-iodide symporter (NIS) mRNA and protein, and the binding of iodine-125-labelled bTSH in cultured porcine thyrocytes. Combination of TSH and c6·5 µM retinol increased iodide uptake and protein iodination compared with TSH alone over the entire incubation time, whereas TSH plus d13 µM retinol increased the uptake of iodine-125 only during the first 12 h but decreased it after 30 h and longer. After d30 h incubation times with d13 µM retinol, the fraction of apoptotic cells was enhanced and proliferation decreased. The incubation with retinol enhanced the binding of [125 I]bTSH to thyrocytes, but did not influence expression of the NIS. With low retinol concentrations, the effect on the binding of TSH apparently predominated and retinol increased thyroid function; with higher concentrations the pro-apoptotic effect of retinol overlapped and a two-phased time course resulted. It can be concluded that low concentrations of retinol also exert differentiating effects in normal thyrocytes.

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“…31 In contrast, HL-60 cell differentiation induced with two different agents, ATRA and PMA was previously shown to decrease the activity of another phospholipase, PIP 2 -PLC. [31][32][33] The specific roles of each PLD isoform in the functions of differentiated myeloid cells are not yet documented. However, levels of PLD1 after HL-60 maturation and differentiation with several inducers suggest that this isoform might be that required for neutrophil and monocyte functions.…”

Section: Discussionmentioning

confidence: 99%

Modifications in phospholipase D activity and isoform expression occur upon maturation and differentiation in vivo and in vitro in human myeloid cells

et al. 2000

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Activation of phospholipase D (PLD) occurs in response to various stimuli and results from the activity of two isozymes, hPLD1 and hPLD2. PLD activity appears to be involved in several myeloid cell processes during their development and activation, including proliferation of myeloblasts in the bone marrow and secretion, phagocytosis and NADPH oxidase activation, essential functions of differentiated neutrophils. The present work studies PLD characteristics, activity and both isozyme expression during maturation and differentiation of myeloid cells by using three different systems: leukemic myeloblasts at different stages of maturation, terminally differentiated neutrophils ex vivo and four human myeloid cell lines, NB4, HL-60, PLB 985 and U937, induced to differentiate with alltrans retinoic acid (ATRA), a cyclic adenosine monophosphate (cAMP) analogue or both agents together. HL-60, a bipotential cell line has also been differentiated along the granulocytic pathway with DMSO and the monocytic pathway with 1,25-dihydroxy vitamin D3. In all these systems, PLD activity increases with maturation and differentiation whatever the inducer used and the granulocytic or monocytic pathways. Increase in basal activity which reflects the expression during development of both hPLD1 and hPLD2 appears to be mainly related to the former isozyme expression. Association of PLD characteristic changes with maturation and differentiation was also confirmed using two NB4 clones resistant to these processes. Comparison between PLD characteristics in myeloblasts during maturation and differentiation ex vivo and in vitro in the different cell lines demonstrated that NB4 induced to differentiate with ATRA represents the best model for further studies on the specific roles of each PLD isoform in various functions of differentiated myeloid cells.

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The differentiating agent, retinoic acid, causes an early inhibition of inositol lipid-specific phospholipase C activity in HL-60 cells

Cited by 19 publications

References 34 publications

Retinoid‐mediated stimulation of steroid sulfatase activity in myeloid leukemic cell lines requires RARα and RXR and involves the phosphoinositide 3‐kinase and ERK‐MAP kinase pathways

Retinoid‐mediated stimulation of steroid sulfatase activity in myeloid leukemic cell lines requires RARα and RXR and involves the phosphoinositide 3‐kinase and ERK‐MAP kinase pathways

Retinol has specific effects on binding of thyrotrophin to cultured porcine thyrocytes

Modifications in phospholipase D activity and isoform expression occur upon maturation and differentiation in vivo and in vitro in human myeloid cells

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