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Biomedical subjects

B Croizat

Publications and source records attributed to B Croizat.

At least 19 recordsLinked to original sources
PubMed1997

Degeneration of cocultures of spinal muscular atrophy muscle cells and rat spinal cord explants is not due to secreted factors and cannot be prevented by neurotrophins.

We have shown recently that cocultures of muscle cells from infantile spinal muscular atrophy (SMA) patients innervated by motoneurons of normal rat spinal cord explants undergo a degeneration process, suggesting that muscle may play a role in this atrophy, which previously has been considered to be a pure motoneuron disease. Conditional media of SMA cocultures did not affect control healthy nerve muscle cocultures. Conversely, conditioned media of control cocultures were unable to prevent degeneration of SMA cocultures. Moreover, neurotrophic factors, thought to be of help in motoneuron disease treatment, did not protect SMA cocultures from premature death. Our results suggest that the abnormal phenotype observed in nerve-muscle coculture (1) is not due to the release of a toxic factor nor to the lack of a secreted survival factor, and (2) does not respond to neurotrophin treatment.

Animals↗
PubMed1996

Neurotrophins increase motoneurons' ability to innervate skeletal muscle fibers in rat spinal cord--human muscle cocultures.

Neurotrophins, nerve growth factor (NGF), neurotrophin-3 (NT-3), neurotrophin-5 (NT-5) and brain-derived neurotrophic factor (BDNF), were studied in vitro in a coculture model of human skeletal muscle myotubes and rat embryo spinal cord explants, which enables the different steps of functional innervation to be followed, including neurite outgrowth, synapse formation and induction of contractile activity. We found that NT-3, NT-5, BDNF, but not NGF simultaneously induced a significant increase in the number and length of neurites emerging from spinal cord explants, the number of endplates per muscle fiber, and the area of innervated muscle fibers around each spinal cord explant. These results suggest that neurotrophins NT-3, NT-5 and BDNF enhance spinal cord motoneurons potential of innervation.

Animals↗
PubMed1995

Constitutive muscular abnormalities in culture in spinal muscular atrophy.

To explore the cause of spinal muscular atrophy (SMA), we used an in-vitro model of nerve-muscle co-cultures in which motoneurons were normal and satellite cells were obtained from SMA patients. In co-cultures initiated with satellite cells from type I and type II SMA patients only, we observed degeneration of the innervated fibres after 1-3 weeks of nerve-muscle co-culture. This process involved vacuolisation, disorganisation, and death of the innervated muscle fibres. This observation points to a muscular implication in the severe forms of SMAs.

Culture Techniques↗
PubMed1994

[Changes of some proteins expression of the spinal cord and muscles in infantile spinal muscular atrophy].

The various types of childhood spinal muscular atrophy (SMA) represent a spectrum of clinical disorders resulting from the degeneration of motor neurons (MN). The genetic defect has been recently localized to chromosome 5q in the region 11.2-13.3. Under normal conditions, half of the motor neurons die during embryonic development, while the remaining 50% survive to innervate muscle fibers and form neuromuscular junctions. Numerous studies using in vivo and in vitro models have shown that survival of MNs depends on the presence of trophic factors of neuronal and muscular origin. However, at the present time, no molecular mechanisms can be proposed to account for the nature and the sequence of the interactions leading to the formation and maintenance of a functional neuromuscular junction. To gain a better understanding of the SMA disorders, an alternative to genetic studies consists in analyzing the molecular mechanisms underlying this pathology. Variations in the expression of proteins, for instance, might reflect the pathological phenotype. We thought it possible to detect differences in the protein(s) which would correlate with the molecular deficit of childhood SMA. We, therefore, compared the patterns of human protein expression from normal controls and SMA spinal cord and muscle. Significant variations in the expression of some proteins, which have been quantified by a computerized Bio-Image electrophoresis system, have been found. In particular, two proteins, a and b (126 kDa and 112 kDa) which are very probably common to spinal cord and muscle show a marked increase of their expression in children with SMA.(ABSTRACT TRUNCATED AT 250 WORDS)

Child↗
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↗