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B Boilly

Publications and source records attributed to B Boilly.

At least 55 records · Page 3Linked to original sources
PubMed1992

Primary structure of neutral and acidic oligosaccharide-alditols derived from the jelly coat of the Mexican axolotl. Occurrence of oligosaccharides with fucosyl(alpha 1-3)fucosyl(alpha 1-4)-3-deoxy-D-glycero-D-galacto-nonulosonic acid and galactosyl(alpha 1-4)[fucosyl(alpha 1-2)]galactosyl(beta 1-4)-N-acetylglucosamine sequences.

Six major neutral and acidic oligosaccharide-alditols were prepared from the jelly coat of Mexican axolotl eggs. These compounds were demonstrated to contain 3-deoxy-D-glycero-D-galacto-nonulosonic acid (dNloA) and L-fucose (Fuc). The structures of the six major oligosaccharides were established as follows: [sequence: see text]

Ambystoma↗
PubMed1992

Increased protein kinase C activity in the central nervous system of the newt during limb regeneration.

Protein kinase C (PKC) activity was examined in the CNS of the newt Pleurodeles waltlii undergoing regeneration after limb amputation. In the spinal cord and brain of control newts, the level of PKC activity was virtually the same for the cytosolic and the particulate fractions. At days 7 and 14 after amputation of two limbs, a twofold increase in overall PKC activity occurred in the spinal cord and accounted for increased membrane-bound activity, while cytosolic activity was not significantly impaired. In contrast, overall PKC activity was not affected in brain. However, a twofold increase in the brain particulate fraction occurred at day 14 while cytosolic activity decreased proportionately. Similar alterations were observed in newts undergoing one or multiple limb amputations. Such changes in PKC activity neither occurred in the CNS of newt after limb denervation nor in the CNS of limb amputated frog Rana temporaria, an Amphibian which is unable to regenerate. Taken together, these results provide evidence that PKC of the CNS is involved in the regeneration process of newts. Changes in activation-associated PKC distribution proceeded through different mechanisms: long-lasting increase in membrane bound activity with a net increase of overall activity in the spinal cord, and long-term redistribution of enzyme activity to the particulate fraction in brain.

Amputation, Surgical↗
PubMed1992

Characterization of Le(x), Le(y) and A Le(y) antigen determinants in KDN-containing O-linked glycan chains from Pleurodeles waltlii jelly coat eggs.

Novel acidic oligosaccharides were isolated in large amounts by reductive alkaline treatment of the jelly coat of Pleurodeles waltlii (Michah) eggs. The oligosaccharides were found to contain the newly described KDN as acidic monosaccharide and possess either the Le(x), Le(y) and A Le(y) antigenic determinants. Occurrence of Le(x) and Le(y) determinants previously recognized as tumor-associated antigen (TAA) demonstrates that mucins of lower animals may represent a rich and easily available source for preparing TAA. Moreover, it reinforces the hypothesis according to which TAA are evolution markers.

Animals↗
PubMed1992

High and low affinity membrane binding sites for fibroblast growth factors in the developing chick brain.

Acidic and basic fibroblast growth factors (aFGF and bFGF), two mitogenic, neurotrophic and angiogenic molecules, are present in the embryonic chick brain but their function remains unclear. In order to approach the biological activity of FGFs during brain development, we have looked for their receptors and studied their regulation through chick brain development. Competitive binding studies realized on brain membranes indicated the presence of two classes of FGF binding sites: high affinity binding sites (dissociation constant, Kd = 100 pM) and low affinity binding sites (Kd = 20 nM). Cross-competition experiments show that these two classes of binding sites both interact with aFGF and bFGF. The number of sites in these two classes of binding sites changes during embryogenesis. On the one hand, the membrane capacity of high affinity sites decreases from E7 (1 +/- 0.2 pmol/mg of protein) to E15 (0.5 +/- 0.2 pmol/mg of protein); on the other hand, the membrane capacity of low affinity sites increases from E15 (25 +/- 4 pmol/mg of protein) to P1 (75 +/- 20 pmol/mg of protein). Cross-linking experiments revealed the presence of two putative receptor forms of molecular masses of about 130 and 95 kDa. These results suggest that the biological activity of aFGF and bFGF during brain embryogenesis could be regulated by the expression of high and low affinity binding sites for these growth factors.

Animals↗
PubMed1992

Basic fibroblast growth factor (bFGF): mitogenic activity and binding sites in human breast cancer.

We investigated binding characteristics of basic fibroblast growth factor (bFGF) on membranes prepared from 4 human breast cancer cell lines and 38 primary BC biopsies. Competitive binding experiments were performed and analyzed using the "Ligand" program. Furthermore bFGF mitogenic activity was measured by [3H]thymidine incorporation into DNA from breast cancer cell lines. The presence of high-affinity binding sites was demonstrated in each cell type (MCF-7: Kd = 0.60 nM; T-47D: Kd = 0.55 nM; BT-20: Kd = 0.77 nM; MDA-MB-231: Kd = 0.34 nM). The presence of these high-affinity binding sites was confirmed with saturation experiments. A second class of low-affinity binding sites was detected in the 2 hormone-independent cells (BT-20: Kd = 2.9 nM; MDA-MB-231: Kd = 2.7 nM). bFGF stimulated the proliferation of MCF-7, T-47D, BT-20 but not MDA-MB-231 cell lines. With competition experiments, binding sites were detectable in 36/38 breast cancers; high-affinity binding sites (Kd less than 1 nM) were present in 19/36 cases and low-affinity binding sites (Kd greater than 2 nM) were present in 29/36 cases (the two classes of binding sites were present in 12 breast cancers). No relation between bFGF binding sites and node involvement, histologic type or grading of the tumor was evidenced. There were negative correlations (Spearman test) between total bFGF binding sites and estradiol receptor (P = 0.05) or progesterone receptor (P = 0.009). The demonstration of (1) bFGF specific binding sites in breast cancer membranes, and (2) bFGF growth stimulation of some breast cancer cell lines indicates that this factor may be involved directly in the growth of some breast cancers.

Adult↗
PubMed1991

Developmental changes of acidic fibroblast growth factor (aFGF) transcription and expression in mouse brain.

In order to increase our knowledge of the in vivo role of acidic fibroblast growth factor (aFGF) in the central nervous system, we have examined aFGF levels during mouse brain development. Using a specific polyclonal antibody raised against aFGF, we measured levels of aFGF-immunoreactive material (IRMaFGF) in extract of total mouse brain taken at different days of development. We found that the level of measurable IRMaFGF remained low and without significant variation during fetal brain development (0.2 ng/mg of extracted proteins). During the first 11 days postnatal (P0 to P11), IRMaFGF increased from 0.5 to 1.5 ng/mg. Between P11 and P14 IRMaFGF levels went up more rapidly, reaching 5 ng/mg. From P30 to adulthood a constant value of 2.5 ng/mg was measured, aFGF content in the different brain extracts was further characterized by its affinity for heparin-Sepharose, its elution at 1 M NaCl from this column and its capacity to induce thymidine incorporation in quiescent fibroblasts. These results were confirmed at the mRNA level. Northern blot analyses of poly A+ mRNA from brains with a specific riboprobe for bovine aFGF, revealed a major 4.5-Kb transcript and a minor 2.7-Kb transcript detectable only in postnatal brains. A similar pattern to that observed for IRMaFGF was seen with these mRNA transcripts, indicating that these aFGFmRNA are translated in the mouse brain. Our results suggest that aFGF may act in the postnatal phases of brain maturation.

Animals↗
PubMed1991

Acidic fibroblast growth factor is present in regenerating limb blastemas of axolotls and binds specifically to blastema tissues.

The growth of regenerating limbs of amphibians depends upon proliferation of the blastema cells that accumulate beneath the epidermal cap. The epidermal cap is known to be mitogenic for the blastema cells. We have extracted a mitogenic activity from both the mesenchymal and epidermal (epidermal cap) components of cone stage blastemas which is retained on heparin-Sepharose and elutes with 1.15 M NaCl. This fraction stimulates neurite outgrowth of PC12 cells and [3H]thymidine incorporation into CCL 39 cells and is potentiated by heparin. The 2 M fraction was inactive. The heparin-Sepharose-purified growth factor cross-reacts with bovine acidic FGF polyclonal antibodies and shows a Mr of 16,000 on Western blots. Blastema membranes contain specific high affinity binding sites (Kd = 25 pM; capacity = 30 fmole/mg protein) and low affinity binding sites (Kd = 18 nM; capacity = 30 pmole/mg protein) for aFGF as revealed by Scatchard analysis. 125I-aFGF which is bound specifically by both the epidermal cap and mesenchyme of blastema frozen sections is displaced by an excess of unlabeled factor and inhibited by heparin. Heparinase treatment and 2 M NaCl washing which decreased the binding was fourfold more efficient for epidermal cap than for mesenchyme suggesting the presence of high affinity receptors in the latter tissue. The presence of aFGF (or a closely related molecule) in blastemas is consistent with our earlier results that showed stimulation of proliferation of cultured blastema cells by acidic or basic FGF or heparin alone. These results suggest the possibility that aFGF is stored in the epidermal cap during limb regeneration and that it stimulates the proliferation of the underlaying mesenchyme.

Ambystoma↗
PubMed1991

Demonstration of basic fibroblast growth factor high and low affinity binding sites in human breast cancer cell lines.

The binding characteristics of basic fibroblast growth factor (bFGF) to membranes prepared from four human breast cancer cell lines (BT-20; MCF-7; MDA-MB-231; T-47D) have been investigated. Scatchard analyses of competition experiments indicate one class of specific binding sites in MCF-7 and T-47D cells, and two classes of specific binding sites in BT-20 and MDA-MB-231 cells. The presence of high affinity sites was demonstrated in each cell type. These results have been confirmed using saturation experiments. Chemical crosslinking of labeled bFGF in breast cancer cell lines followed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) revealed one specific complex with a relative molecular mass of about 85,000. A second class of lower affinity binding sites was detected only in the two hormone-independent cell lines. bFGF stimulation of proliferation has also been demonstrated in MCF-7, T-47D, and BT-20, but not in MDA-MB-231, which has a high proliferation activity without the addition of growth factors. These suggest that the presence of bFGF specific binding sites in human breast cancer cell membranes is a necessary but not sufficient condition for exogenous bFGF growth stimulation of these cells; they also suggest that FGF plays a role in breast cancer.

Breast Neoplasms↗
PubMed1990

Distribution of intravenously administered acidic and basic fibroblast growth factors in the mouse.

Iodinated acidic or basic fibroblast growth factor (aFGF or bFGF) were separately injected into adult mice to follow their distribution in the main organs of the animals. Iodinated FGFs intravenously injected into mice cleared from blood with a T1/2 of 30 s. They mainly bound to kidney, liver and spleen. The binding of FGFs to these organs was maintained when the latter were washed with a physiological buffer containing 0.15 M NaCl, but it was eliminated when the buffer contained 2 M NaCl. Simultaneous injections of the FGFs together with increasing doses of heparin weakened the binding of FGF to vessels in a dose-dependent manner.

Animals↗
PubMed1990

Evidence of high and low affinity binding sites for basic fibroblast growth factor in mouse placenta.

The placenta has been shown to contain bFGF, but the presence of specific binding sites for this growth factor in this tissue remained to be established. In order to study the role of bFGF in the placenta growth, we looked for specific binding sites on mouse placental cell membranes at days 12, 14, 16, and 18 of pregnancy. At day 12, Scatchard analyses indicated that two classes of specific interaction sites for bFGF were detected. One class of high affinity binding sites was characterized by an apparent Kd of 10 pM and a binding capacity of 10 fmoles per mg of membrane protein. A second class of low affinity binding sites was detected with an apparent Kd of 60 nM and a binding capacity of 26 pmoles per mg of membrane protein. At days 14, 16 or 18, Scatchard analyses only showed low affinity binding sites with an apparent Kd of 24 nM and a binding capacity of 230 pmoles per mg of membrane protein. The characterization of these binding sites was performed by cross linking experiments that revealed two forms of specific complexes. This result suggested that the high affinity binding sites correspond to putative receptors with relative molecular masses equal to 65,000 and 85,000. The dramatic decrease of the high affinity receptor number after the 12th day of pregnancy, which is synchronous with the 9-fold increase of the low affinity binding site number, suggests that the biological activity of bFGF could be regulated by a balance between both the numbers of high and low affinity binding sites on placenta cell membranes. Thus, as it was shown for other growth factors, bFGF could only be involved at specific pregnancy stages.

Animals↗
PubMed1990

Cell interactions and regeneration control.

This paper is a review of the main findings of our laboratory on the control of regeneration by cell interactions. These include results related to the role of both cell contact and local soluble factors in regeneration of the legs of insects and newts and of the parapodia and segments of nereis. The pattern of these structures is considered to be defined by positional information distributed as longitudinal and transverse positional value sequences carried by epidermal (insect) or mesenchymal (newt) cells. By associating tissues to create transverse and longitudinal discontinuities in these sequences, single or multiple regenerating structures were obtained. These structures are formed by the intercalation of cells characterized by intermediate positional values which fill the gap between the tissues in contact. Positional information may also be changed during regeneration by the nerve cord in nereis and retinoids in the newts. We describe additional cases where morphogenesis occurs without any overt discontinuity in positional information, such as from a locally injured or non-injured insect trochanter, or after deflection of nerves in nereis and newt. Regeneration following an amputation may be considered as a special case of intercalary regeneration, the first stage being the juxtaposition of normally non-contiguous cells resulting in a longitudinal or/and a transverse gap. We also report studies on local factors produced by nerves and the blastema during newt limb regeneration. The nerve factor is necessary for the division of blastemal cells. After denervation, mesenchyme differentiates in an abnormal way. The mitogenic signal from the nerves is mediated by the PKC pathway. Its production is enhanced by regeneration of cut nerve fibers. The blastema also produces growth factors. We show that the epidermal cap and mesenchyme contain acidic FGF-like factor, and that the proliferating mesenchyme stimulates nerve fibers to regrow into the blastema.

Amphibians↗
PubMed1988

Production in vitro by spinal cord of growth factor(s) acting on newt limb regeneration: influence of regeneration of the nerve fibers.

In order to approach the problem of regulation of growth factor(s) production during limb regeneration in newt, we co-cultivated spinal cord segments and blastemas. First we showed that, like the sensory supply, the spinal cord possesses size-dependent mitogenic capacities for limb blastemas. A 5-mm long spinal segment enhances radiolabelled thymidine incorporation to the same extent as spinal ganglia (1.6-fold). Second, we co-cultivated blastemas with spinal segments, the nerve fibers of which were previously stimulated to regenerate (= stimulated spinal segment) or not (= non-stimulated spinal segment). Only after a 24-h coculture, do stimulated spinal segments enhance thymidine incorporation in blastemas 2-fold more than non-stimulated spinal segments. Our results suggest that during limb regeneration brachial nerves produce more growth factor(s) when regrowing, inducing the proliferation of blastema cells which in return deliver a neuronotrophic factor acting on these nerves.

Animals↗
PubMed1988

Blastema cell proliferation in vitro: effects of limb amputation on the mitogenic activity of spinal cord extracts.

Primary cultures of mesenchymal cells of axolotl limb blastemas provide a very sensitive in vitro bioassay for studying nerve dependence of newt regeneration. These cells can be stimulated by crude spinal cord extracts of non-amputated animals in a dose-dependent manner up to 60 micrograms protein/ml of culture medium; at this concentration the mitotic index is increased 4-fold. Spinal cord extracts of axolotls 14 days after forelimb amputation (i.e., late bud stage) are more efficient in stimulating blastema cell proliferation (+50%) than extracts of axolotls 7 days after forelimb amputation (i.e., early bud stage) or of axolotls without amputation. In a similar manner, spinal cord extracts of young axolotls 14 days after forelimb amputation, are more stimulatory than older axolotls 14 d after forelimb amputation which regenerate only a very small blastema during the same time. It appears that spinal cord mitogenic activity is enhanced after limb amputation, probably in correlation with blastema cell requirements for limb regeneration.

Ambystoma mexicanum↗