Biomedical subjects

N Bachnou

Publications and source records attributed to N Bachnou.

4 recordsLinked to original sources

PubMed1996

An identical effect mediated by thyroid deficiency or oncogene v-erbA in the chick embryo.

We have shown earlier that the association of v-myc and v-erbA (MAHEVA construct) is responsible for the appearance of a specific phenotype in chick embryos inoculated at E3. This phenotype comprises rapidly growing heart rhabdomyomas (induced by v-myc alone) and within these tumors secondarily appearing cartilage nodules (Bachnou et al., Oncogene 6: 1041-1047, 1991). Here we report that v-erbA can be replaced by thyroid deficiency. When decapitated embryos were inoculated with virus MC29 (v-myc alone) or when v-myc inoculated embryos were treated with thiourea, 100% of the embryos reaching E17 to E19 displayed tumoral hearts bearing cartilage nodules. We thus report in vivo evidence that v-erbA acts by antagonizing the effects of thyroid hormones. Remarkably, thyroid deficiency rendered embryos more sensitive to the effect of v-myc, since 100% developed heart rhabdomyomas and cartilage nodules, versus about 70% affected when either v-myc or MAHEVA were inoculated. Thyroid deficiency did not alter the species-specific character of transdifferentiation, since only chick but not quail embryos developed cartilage nodules after thyroidectomy or MAHEVA infection.

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PubMed1991

MC29-immortalized clonal avian heart cell lines can partially differentiate in vitro.

We established quail clonal heart muscle cell lines from cardiac rhabdomyosarcomas developed in embryos injected in ovo with the MC29 virus containing the v-myc oncogene. These clones were characterized by means of antibodies detecting markers of striated muscle cells. Two clones were selected for further characterization on the basis of a distribution of myogenic markers similar to that in normal early embryonic cardiac muscle cells. However, these muscle markers progressively disappeared with time in culture. Cardiomyocytic differentiation could be reinduced in culture, by associating the avain cardiac cells with 3T3 cells in a defined synthetic medium. Muscle markers were then reexpressed in all cardiac cells as soon as Day 1 after coculture. Multiplication of cardiac cells continued at the same time. This is characteristic of cardiac clones since MC29-infected quail myoblasts and MC29-infected quail fibroblasts exhibited a split response to 3T3 association, i.e., decreased growth and enhanced differentiation. The cardiac clones were maintained in vitro for more than 60 generations (6 months) without morphological changes. To our knowledge, this is the first description of clonal embryonic avian heart cell lines.

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PubMed1991

Cooperative effect of v-myc and v-erbA in the chick embryo.

We show that a construct designated as MAHEVA, which encodes oncogenes v-myc from MH2 virus and v-erbA from AEV under the control of the LTR of MH2, induces rapidly growing heart rhabdomyosarcomas, when it is injected in E3 but not E5 chick embryos. A similar pathology has previously been observed with MC29, within the same limited time frame. The tumors, which expressed P61-63myc, P75gag-erbA and Pr76gag proteins were detectable from E14 onwards. Compared with MC29, MAHEVA induced a secondary anomaly, not detectable prior to E17. This is the appearance of cartilage nodules within the heart rhabdomyosarcomas. The constant location of these nodules inside the rhabdomyosarcomas and their delayed appearance suggests that the chondrocytes originate from myoblasts prevented from differentiating by the expression of the v-myc product. This interpretation is supported by the appearance of chondrocytes in E3 heart muscle cells infected in vitro with MAHEVA.

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PubMed1990

Oncogenes and avian development.

In order to detect signs of oncogene activity and elucidate their possible role in avian ontogeny we implemented two different strategies. One was to detect either the protein product or messenger RNA in situ at various stages of development. The other was to try and disturb development with retroviruses carrying one or several oncogenes in their activated forms. Time- and tissue-specific expression of c-myc was apparently not related to particular phases of cell evolution, such as population amplification. Rather the presence of c-myc immunoreactive product at particular stages appeared to depend on cell types. c-myb and c-ets messenger RNAs were found expressed preferentially in the blood system, respectively in hemopoietic and differentiating endothelial cells. The developing embryo heart was found to be uniquely sensitive to the effect of retroviruses provided that two conditions were respected. The first was the injection of the virus or construct prior to E3.5. The second was the presence of the v-myc gene, whether alone or associated with one or several other v-onc. In such cases a large proportion (70%) of chick and all quail embryos developed multiple heart rhabdomyosarcomas within 10 days. In chickens the association of a second v-onc or of two others induced the formation of secondary tumors, whose type was determined by the nature of the other oncogene(s).(ABSTRACT TRUNCATED AT 250 WORDS)

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