Inhibition of dimethylsulfoxide-induced differentiation in friend erythroleukemic cells by diacylglycerols and phospholipase C

Pincus, SM; Beckman, Barbara S.; George, William J.

doi:10.1016/0006-291x(84)90567-9

Cited by 15 publications

(4 citation statements)

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“…It has been reported that phospholipase C (PLC) beta 1 is down‐regulated during the (incomplete) erythroid maturation of Friend erythroleukemia cells; moreover, PLC beta overexpression in these cells inhibited differentiation in response to DMSO (79). In line with these findings, PLC beta mRNA abundance strongly decreased at 20 h in our screen and was even further down‐regulated at 48 h.…”

Section: Resultsmentioning

confidence: 99%

Establishment of normal, terminally differentiating mouse erythroid progenitors: molecular characterization by cDNA arrays

Dolznig

Boulmé²,

Stangl³

et al. 2001

FASEB j.

121

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Expression profiling with cDNA arrays is an excellent tool for molecular analysis of complex processes such as terminal erythroid differentiation. The shortcomings of the currently available erythroid in vitro differentiation models, however, severely impaired the usefulness of this approach to study erythropoiesis. Here, we describe a novel, murine erythroid cell system closely corresponding to in vivo erythroid progenitors. Mortal, long‐term proliferating erythroid progenitors of fetal liver or immortal strains of p53‐deficient erythroblasts were established in culture. Both cell types proliferated in serum‐free medium and were strictly dependent on physiologically relevant cytokines and hormones, stably retaining a diploid set of chromosomes. If exposed to physiological differentiation factors (erythropoietin plus insulin), cells synchronously recapitulated the normal in vivo differentiation program to mature terminally into enucleated erythrocytes and expressed stage‐specific erythroid transcription factors in the expected temporal order. Using cDNA arrays, we found a large number of genes differentially expressed at time points during differentiation. Already 6 h after differentiation induction, 17% of the expressed genes showed significant alterations in mRNA abundance, increasing to 53% (12% up‐regulated, 41% down‐regulated genes) by 48 h. Cluster analysis of mRNA expression kinetics during differentiation identified six distinct expression patterns. All genes on the array with a known function in erythropoiesis showed the expected variations in expression. The genes identified also allowed first insights into the sequence of events within the regulatory network responsible for erythroid maturation. In mortal wild‐type as well as immortal p53‐/‐ erythroblasts, changes in mRNA abundance of several well‐regulated gene products was verified at the protein level. Taken together, this novel hematopoietic cell system faithfully executes essential steps of normal erythropoiesis and allows us to dissect and characterize molecular mechanisms involved in erythropoiesis.

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Section: Resultsmentioning

confidence: 99%

Establishment of normal, terminally differentiating mouse erythroid progenitors: molecular characterization by cDNA arrays

Dolznig

Boulmé²,

Stangl³

et al. 2001

FASEB j.

121

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“…Since DAG activates PKC (129), this implies that the effects of DMSO and HMBA may be brought about by perturbations in cell membrane structure which in turn can inhibit PKC. Indeed, in leukemic cell lines, DAG inhibits DMSO-induced differentiation (130). However, inhibition of PKC alone cannot be the sole initiator of differentiation since the phorbol diester 12-0-tetradecancyl-phorbol-13-acetate, which activates PKC (131), can also induce morphologic and biochemical differentiation in some cells, including NB (132)(133)(134)(135).…”

Section: Butyric Acidmentioning

confidence: 99%

Human neuroblastoma cell lines as models for the in vitro study of neoplastic and neuronal cell differentiation.

Abemayor¹,

Sidell²

1989

Environ Health Perspect

143

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Neuroblastoma is a childhood solid tumor composed of primitive cells derived from precursors of the autonomic nervous system. This neoplasm has the highest rate of spontaneous regression of all cancer types and has been noted to undergo spontaneous and chemically induced differentiation into elements resembling mature nervous tissue. As such, neuroblastoma has been a prime model system for the study of neuronal differentiation and the process of cancer cell maturation. In this paper we review those agents that have been described to induce the differentiation of neuroblastoma, with an emphasis on the effects and possible mechanisms of action of a group of related compounds, the retinoids. With this model system and the availability of subclones that are both responsive and resistant to chemically induced differentiation, fundamental questions regarding the mechanisms and processes underlying cell maturation have become more amenable to in vitro study.

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“…Cells were then washed twice in Ca2+-, Mg2+-free MEM and seeded at 100,000 celldm1 in 25 mm2 culture flasks. At the indicated times after seeding, viability was assessed with trypan blue exclusion, and the cells were stained for hemoglobin using 3',3'-diaminobenzidine (Pincus et al, 1984). Most experiments were repeated three to four times with duplicate flasks, for each condition.…”

mentioning

confidence: 99%

Superoxide dismutase induces differentiation of friend erythroleukemia cells

Beckman

Balin

Allen

1989

Journal Cellular Physiology

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Friend erythroleukemia cells (FELC) served as a model system for cell differentiation because these cells can be triggered to differentiate by a variety of chemical agents. Treatment with the classical inducer of differentiation, hexamethylene bisacetamide (HMBA), stimulated superoxide dismutase (SOD) activity, which increased in parallel with HMBA-induced differentiation. Furthermore, FELC were shown to differentiate in response to the addition of liposomes containing SOD. Oxidative treatment with liposomes containing D-amino acid oxidase or xanthine oxidase, cumene peroxide, or potassium superoxide also induced differentiation, whereas antioxidants such as alpha-tocopherol, butylated hydroxytoluene, or beta-carotene did not induce differentiation. Also, HMBA induction of differentiation was suppressed by treatment with antioxidants.

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Inhibition of dimethylsulfoxide-induced differentiation in friend erythroleukemic cells by diacylglycerols and phospholipase C

Cited by 15 publications

References 5 publications

Establishment of normal, terminally differentiating mouse erythroid progenitors: molecular characterization by cDNA arrays

Establishment of normal, terminally differentiating mouse erythroid progenitors: molecular characterization by cDNA arrays

Human neuroblastoma cell lines as models for the in vitro study of neoplastic and neuronal cell differentiation.

Superoxide dismutase induces differentiation of friend erythroleukemia cells

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