Quantitative morphological aspects of granulocytic differentiation induced in HL-60 cells by dimethylsulfoxide and retinoic acid

Dufer, Jean; Biakou, Daniel; Joly, Philippe; Benoist, Hervé; Carpentier, Y.; Desplaces, A

doi:10.1016/0145-2126(89)90131-8

Cited by 18 publications

(9 citation statements)

References 14 publications

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“…In cases when hepatocellular dysplasia was caused by treatment with secondary bile acids, the rate of nuclear polymorphism was higher as compared to controls. Similar observations of the increase of polymorphism of cytological characteristics of malignant cells were described in other organs (4,12) and in cells cultured in vitro (11).…”

Section: Discussionsupporting

confidence: 86%

“…This latter parameter was also used to distinguish normal and perineoplastic skin in women (9). Differences in nuclear geometry and the number of cytoplasmic granules were described in HL-60 cells cultured in medium containing inducers of differentiation such as dimethyl sulfoxide and retinoic acid (11). Cell shape polymorphism was used as a diagnostic parameter to distinguish between two lines of human prostate cancerous cells (7).…”

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confidence: 99%

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Nuclear polymorphism and nuclear size in precarcinomatous and carcinomatous lesions in rat colon and liver

Zusman¹,

Kozlenko²,

Zimber

1991

Cytometry

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The role of nuclear polymorphism and nuclear size in an analysis of the differences between colon and liver tumors in rats as well as in an analysis of hepatic dysplasia was studied. It was shown that colon tumors which developed following treatment of animals with a direct carcinogen alone or with a carcinogen followed by secondary bile acid were characterized by low incidence of nuclear polymorphism and by an increased nuclear size in epithelial cells. Metastatic liver tumors in rats with colon tumors were characterized by a high value for the coefficient of nuclear form polymorphism and by a significant decrease in nuclear size. Hepatic dysplasia which developed as a result of prolonged treatment with secondary bile acids was characterized by high rate of nuclear form polymorphism and by a significant increase in nuclear size. The obtained results suggest that nuclear polymorphism is dependent upon the type of tissue or organ involved in the cancerous transformation and that it may have significance as a diagnostic marker of precarcinomatous and carcinomatous lesions of digestive organs only when used in combination with other analyses.Key terms: Rat colon and liver tumors, hepatic dysplasia, nuclear form polymorphism, coefficient of polymorphismIn spite of the extensive use of histochemistry and immunohistochemistry in clinical histopathological practice, light microscopical morphometry also provides important information (24). For example, parameters such as cellular and nuclear areas, nuclear-cytoplasmic, and nucleolar-nuclear ratios have been utilized to characterize hepatocellular dysplasia (17). It was shown that morphometric examination complements histological evaluation and allows dysplastic cells to be identified (27). A correlation between nuclear size and the type of lung carcinoma (3,10,16) as well as prognosis i n breast cancer (20) has been shown. Nuclear perimeter and nuclear optical density were shown to have diagnostic significance in identifying transformed cells of cervical carcinomas (51, salivary gland tumors (15), gastric carcinoma (21), or prostate carcinomas (14,191. The determination of shapes of cells and nuclei has been used in a n analysis of human hepatocellular carcinoma (6). It was shown, for example, that nuclear polymorphism is one of the characteristics of liver cell dysplasia (1,2), the first stage of which is characterized by enlarged nuclei and a n increased nuclear-cytoplasmic ratio (23). This latter parameter was also used to distinguish normal and perineoplastic skin in women (9). Differences in nuclear geometry and the number of cytoplasmic granules were described in HL-60 cells cultured in medium containing inducers of differentiation such as dimethyl sulfoxide and retinoic acid (11). Cell shape polymorphism was used as a diagnostic parameter to distinguish between two lines of human prostate cancerous cells (7).In this communication we studied the relation of nuclear shape and nuclear size to the type of the affected tissue and to the stage of its transformation. Ra...

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Section: Discussionsupporting

confidence: 86%

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confidence: 99%

Nuclear polymorphism and nuclear size in precarcinomatous and carcinomatous lesions in rat colon and liver

Zusman¹,

Kozlenko²,

Zimber

1991

Cytometry

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“…HL‐60 cells were maintained in DMEM medium supplemented with 10% foetal bovine serum, 2 m M L ‐glutamine, 100 μg ml −1 streptomycin and 100 u ml −1 penicillin (Life Technologies, Gaithersburg, MD, U.S.A.). HL‐60 cells were induced to differentiate into either macrophagic cells by culturing in the presence of 20 n M phorbol 12‐myristate 13‐acetate (PMA), or granulocytic cells by co‐culture with 1.2% DMSO, 750 μ M dibutyryl‐cAMP or 1 μ M 13‐cis‐retinoic acid (Sigma, St. Louis, MO, U.S.A.) (Breitman et al ., 1980; Dufer et al ., 1989).…”

Section: Methodsmentioning

confidence: 99%

“…To this end, we assessed putative CCR1 expression and functionality in dierentiated HL-60 cells. HL-60 cells are promeylocytic British Journal of Pharmacology vol 137 (5) Pharmacology of CCR1 C.-C. Chou et al leukaemia cells which can be dierentiated into macrophagic or granulocytic cells by varying their culture conditions (Breitman et al, 1980;Dufer et al, 1989). HL-60 cells were grown in the presence or absence of 20 nM PMA for 2 days to stimulate macrophagic dierentiation or with 1.2% DMSO (3 days), 750 mM dibutyryl-cAMP (3 days) or 1 mM 13-cis-retinoic acid (5 days) to encourage granulocytic dierentiation.…”

Section: Ccr1 Binding and Activation In Ba/f3-ccr1 Membranesmentioning

confidence: 99%

Pharmacological characterization of the chemokine receptor, hCCR1 in a stable transfectant and differentiated HL‐60 cells: antagonism of hCCR1 activation by MIP‐1β

Chou¹,

Fine²,

Pugliese-Sivo³

et al. 2002

British J Pharmacology

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1 C-C chemokine receptor-1 (CCR1) has been implicated in mediating a variety of in¯ammatory conditions including multiple sclerosis and organ rejection. Although originally referred to as the MIP-1a/RANTES receptor, CCR1 is quite promiscuous and can be activated by numerous chemokines. 2 We used radioligand binding and [ 35 S]-GTPgS exchange assays in membranes from a cell line transfected to express CCR1 (Ba/F3-hCCR1) to characterize a panel of chemokines (HCC-1, MIP1a, MIP-1b, MIP-1d, MPIF-1, MCP-2, MCP-3, and RANTES) as CCR1 ligands. In this recombinant model, these chemokines displaced 125 I-MIP-1a with a wide range of potencies and, with the exception of MCP-2, acted as full agonists in stimulating [ 35 S]-GTPgS exchange. 3 We then assessed the utility of HL-60 cells cultured with known di erentiating agents (PMA, DMSO, dibutyryl-cAMP or retinoic acid) for investigating CCR1 pharmacology. In [ 35 S]-GTPgS exchange assays, membranes from cells cultured with retinoic acid (4 ± 6 days) were the most responsive to activation by MIP-1a and MPIF-1. FACS analysis and comparative pharmacology con®rmed that these activities were mediated by CCR1. HCC-1, haemo®ltrate CC chemokine 1; IP-10, interferon-inducible protein of 10 kDa; I-TAC, interferoninducible T cell a chemoattractant; IL-8, interleukin-8; MIP-1a, macrophage in¯ammatory protein-1a; MIP-1b, macrophage in¯ammatory protein-1b; MIP-1d, macrophage in¯ammatory protein-1d; MCP-1, MCP-2, MCP-3, monocyte chemotactic protein-1, -2 and -3; Met-RANTES, methionylated RANTES; Mig, monokine-induced by human interferon g; MPIF-1, myeloid progenitor inhibitor factor-1; NAP-2, neutrophil activating peptide-2; RANTES, regulated upon activation, normal T cell expressed and secreted; WGA-SPA, wheat germ agglutinin bead-scintillation proximity assay

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“…Cultures were initiated with 700 cells/well and each point represents the mean _+ SEM of duplicate samples. (GH), prostaglandins Et and E2, LIF, human IL-9, and IL-11, all of which have been reported to increase erythroid colony numbers in methylcellulose (17-23); and TNF-cq activin, TGF-31, retinoic acid, spermidine, HMBA, DMSO, and the cell cycle blockers thymidine, aphidicolin, and 5-azacytidine, all of which have been shown to induce differentiation in some systems(24)(25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35)(36)(37)(38)(39)(40). We tested these reagents over a wide range of concentrations and the results, shown inTable 1, are those obtained with concentrations that gave the most pronounced effects on differentiation.…”

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confidence: 99%

Transforming growth factor beta 1 is an inducer of erythroid differentiation.

Krystal

Lam

Dragowska

et al. 1994

The Journal of Experimental Medicine

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SummaryNormal human bone marrow cells, highly enriched for burst-forming units-erythroid (BFU-E), were cultured in serum-free medium, in the presence and absence of various factors, to investigate the mechanisms involved in regulating erythroid differentiation. In cultures containing interleukin 3 (IL-3), Steel factor (SF), and erythropoietin (Ep), benzidene-positive erythroblasts first became detectable on day 6. Their numbers then rapidly increased until, by day 16, >99% of the cells, which were 20,000-fold amplified over input numbers, were benzidene-positive. It is interesting to note that omission of either SF or Ep from this assay markedly enhanced the rate of differentiation and reduced total cell numbers, whereas omission of IL-3 had no effect on the rate of differentiation and only slightly reduced cell numbers. Of various agents tested, the most potent erythroid differentiation inducer (and inhibitor of cell proliferation) was found to be transforming growth factor ~81 (TGF-~I). This cytokine stimulated both the rapid appearance of hemoglobin-positive cells and an early cessation of cell proliferation. Using fluorescently tagged antibodies to glycophorin A and fluorescence-activated cell sorter (FACS) analysis, this phenomenon was shown to be due to an early induction of erythroid differentiation rather than an aberrant production of hemoglobin. Methylcellulose assays indicated that the well-documented reduction of BFU-E colony numbers observed with TGF-~31 may actually be due to a TGF-Bl-induced "conversion" of BFU-E into colony-forming units-erythroid (CFU-E). Thus, in vivo, TGF-fll might serve, in part, to decrease the number of mature erythrocytes by stimulating BFU-E to skip a number of cell divisions and differentiate early.

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Quantitative morphological aspects of granulocytic differentiation induced in HL-60 cells by dimethylsulfoxide and retinoic acid

Cited by 18 publications

References 14 publications

Nuclear polymorphism and nuclear size in precarcinomatous and carcinomatous lesions in rat colon and liver

Nuclear polymorphism and nuclear size in precarcinomatous and carcinomatous lesions in rat colon and liver

Pharmacological characterization of the chemokine receptor, hCCR1 in a stable transfectant and differentiated HL‐60 cells: antagonism of hCCR1 activation by MIP‐1β

Transforming growth factor beta 1 is an inducer of erythroid differentiation.

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