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B Croizat

Publications and source records attributed to B Croizat.

At least 19 recordsLinked to original sources
PubMed1992

Growth inhibition of N1E-115 mouse neuroblastoma cells by c-myc or N-myc antisense oligodeoxynucleotides causes limited differentiation but is not coupled to neurite formation.

Antisense oligodeoxynucleotides were found to be stable in the culture medium containing fetal calf serum (heat-inactivated 30 minutes at 65 degrees C) and in cells. Antisense oligomer treatment causes cessation of mitoses, but does not lead to morphological differentiation. Under antisense conditions, we have observed an increase in the amount of two neurospecific protein, namely peripherin and gamma-enolase. Comparison of the results obtained with chemical inducers and antisense oligodeoxynucleotides allows us to postulate three phases in N1E-115 differentiation: the first correspond to the arrest of mitosis, the second to the expression of a limited neuronal program, and the third to the morphological and electrophysiological differentiation.

Animals↗
PubMed1992

Adriamycin promotes neurite outgrowth in the "neurite-minus" N1A-103 mouse neuroblastoma cell line.

Adriamycin, an anticancer agent acting on topoisomerase II, promotes the arrest of cell division and neurite extension in a "neurite-minus" murine neuroblastoma cell line, N1A-103. This morphological differentiation is accompanied by a blockade in the S phase of the cell cycle, modification of the amount of peripherin, and appearance of the beta 7-tubulin isoform. Yet, adriamycin-induced N1A-103 cells fail to express other neuronal markers, such as long-lasting Ca2+ channels, synaptophysin, and the shift in the proportion of the beta'1 tubulin isoform to the beta'2 isoform, whose appearance parallels the terminal differentiation of the wild type neuroblastoma cell line N1E-115. Hence, a comparison of the behavior of these two cell lines leads to the proposal that there are two programs of neuroblastoma differentiation: one where expression is triggered by the arrest of cell division and which is observed in adriamycin-induced N1A-103 variant cells, and the other, presumably occurring further downstream, which would involve further changes in morphogenesis and acquisition of new electrophysiological properties.

Animals↗
PubMed1991

Mitochondrial maturation during neuronal differentiation in vivo and in vitro.

The evolution of the mitochondrion has been followed within differentiating neuronal cells, both in primary cultures of neurons from fetal rat cortex and during rat brain cortex maturation. Changes in total mitochondrial proteins (mt-proteins) were evaluated, and qualitative changes in the mt-proteins pattern were analyzed using the Western blot technique. The evolution of mt-protein contents in cultured neurons resembles what is observed during rat brain maturation. The mitochondrion exhibits pronounced changes in the course of neurogenesis, in particular, bursts of mitochondrial masses accompanying the successive steps of neurogenesis are observed. There are indications that protein equipment of mitochondria during neuronal development undergoes variations. Although more work is required to establish the significance of these correlations, the present data might suggest an important role of the mitochondrion in neurogenesis.

Animals↗
PubMed1991

Regulation of c- and N-myc expression during induced differentiation of murine neuroblastoma cells.

Using clones N1E-115 and N1A-103 from mouse neuroblastoma C1300, a comparative analysis of c- and N-myc gene expression was undertaken both in proliferating cells and in cultures exposed to conditions which induce differentiation. Under the latter conditions, while N1E-115 cells extend abundant neurites and express many biochemical features of mature neurons, clone N1A-103 stops dividing and expresses certain neurospecific markers but is unable to differentiate morphologically. In both clones, chemical agents, i.e. 1-methyl cyclohexane carboxylic acid (CCA) or dimethyl sulfoxide (DMSO), induce a decrease in c-myc expression. Similar results were found for N-myc gene in N1E-115 cells, but in contrast, in clone N1A-103, N-myc expression is increased with CCA and not modified with DMSO. Globally, this study favours the hypothesis that changes in c-myc expression would correspond to cell division blockade and differentiation, while modulations in N-myc are more closely related to an early phase of terminal differentiation.

Animals↗
PubMed1989

Tissue-specific mitochondrial proteins.

Mitochondrial proteins from rat brain cortex, muscle, liver, and from neuronal cells in culture were compared on 2-D electrophoregrams. This analysis permitted characterization of certain specificities in the distribution of polypeptides depending on tissue localization. In particular, 16 mit-proteins were found exclusively in the mitochondrion from brain tissue.

Animals↗
PubMed1987

Changes in the beta-subunit of mitochondrial F1 ATPase during neurogenesis.

A polypeptide migrating in the area of the isotubulin in 2 D-gel electrophoresis of extracts from neuronal cells was characterized as the beta-subunit of the F1 ATPase matrix component. The synthesis of this subunit is enhanced during neurogenesis and the presence of an isoform was detected in adult mouse brain.

Animals↗
PubMed1986

Effects on mitochondrial metabolism of CCA, one inducer of neuroblastoma differentiation.

CCA, a potent neuroblastoma differentiation inducer, was shown by oxygraphic measurements to reduce significantly the O2 consumption of whole neuroblastoma cells as of mitochondria purified from neuroblastoma or mouse cortex. The effect of CCA on the respiration was compared to those of oligomycin. Our results suggest that the molecular target of CCA is the matrix F1 catalytic component of the F0F1 mitochondrial ATPase.

Animals↗
PubMed1984

Changes in mitochondrial proteins during neuroblastoma differentiation.

The evolution of three major mit-proteins was followed in neuroblastoma cells cultured in different conditions of differentiation. 1 methyl cyclohexane carboxylic acid (CCA) was found to stimulate the synthesis of the three mit-protein markers. This result, compared to the effects of oligomycin, an inhibitor of mitochondrial function, favours the hypothesis that CCA induces in vitro neurogenesis through a general metabolic alteration.

Animals↗
PubMed1979

[Morphological differentiation of neuroblastoma by 1 methyl cyclohexane carboxylic acid (CCA) and some C1 derivatives].

We describe the induction of neuroblastoma morphological differentiation by 1 methyl cyclohexane carboxylic acid (CCA) and by some C1 derivatives of CCA. This induction proceeds in a medium which allows, in the absence of inducer, a normal growth of neuroblastoma cells and contains 7.5% fetal Calf serum. In order to establish a clear-dose response relationship and to compare the relative potencies of different drugs, the morphological changes were assessed by examining "long neurite-bearing cells".

Animals↗
PubMed1978

Complexity of polysomal polyadenylated RNA in undifferentiated and differentiated neuroblastoma cells.

Using cDNA probes, we have analysed the sequence complexity and the frequency distribution of the polysomal poly(A)-containing RNA from neuroblastoma cells at two different developmental states: either as round, immature neuroblasts, or as differentiated cells exhibiting the morphological properties of mature neurons. The total complexities measured for mRNA from undifferentiated and differentiated cells are identical and correspond to approximately 7000 average-sized sequences of 1750 nucleotides distributed in the same three abundance classes. We have determined the homology between the mRNA populations corresponding to the two developmental states by heterologous cross-hybridization: all the sequence from differentiated cells are present in the polysomes of undifferentiated cells. Conversely, the mRNA from differentiated cells fails to hybridize with about 15% of hybridizable cDNA corresponding to undifferentiated cells. This difference probably results from the disappearance of some mRNA species and may be related to the terminal differentiation of neuroblastoma cells.

Animals↗
PubMed1977

Poly(A)-containing RNA in neuroblastoma: immature and differentiated cells in culture.

We have analysed the poly(A)-containing RNA from neuroblastoma cells at two different developmental states: either as round, immature neuroblasts grown in suspension, or as differentiated cells exhibiting the morphological properties of mature neurons, when attached to a culture dish. Suspension-grown and monolayer cells were pulse-labelled with tritiated uridine. The profile of cytoplasmic poly(A)-containing RNA from suspension cells is highly heterogeneous with peaks ranging from 16-30 S. The profile obtained from differentiated cells appears somewhat distinct from the previous one. This is evidenced by a relative decrease in the 26-S peak and a virtual disappearance of the 16-S component. In order to compare the 'steady-state' patterns of poly(A)-containing RNA in these two developmental stages, polysomal RNA was prepared from unlabelled cells. Following sucrose gradient sedimentation, each fraction was hybridized to [3H]poly(U). Examination of the two RNA hybridization profiles reveals striking similarities suggesting that 'steady-state' messenger populations include, on the average, the same subspecies. The 16-S fraction, which was not observed after the pulse-labelling of the monolayer culture, is detected here by hybridization to [3H]poly(U) when using polysomal poly(A)-containing RNA from monolayer cells as substrate. These results suggest that terminal differentiation of neuroblastoma cells is not accompanied by major alterations of the transcription program and is paralleled by a marked stabilization of the 16-S species.

Cell Differentiation↗