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Biomedical subjects

M Berreur

Publications and source records attributed to M Berreur.

6 recordsLinked to original sources

Cellular activity and signaling induced by osteoprotegerin in osteoclasts: involvement of receptor activator of nuclear factor kappaB ligand and MAPK.

Osteoprotegerin (OPG) is a decoy receptor for receptor activator of nuclear factor kappaB ligand (RANKL), an inducer of osteoclastogenesis via its receptor RANK. We recently demonstrated that OPG also exerts a direct effect in osteoclasts by regulating protease expression. Herein, we showed that OPG-induced pro-matrix metalloproteinase-9 activity was abolished by ras/MAPK inhibitors in purified osteoclasts. OPG induced the phosphorylation of p38 and ERK1/2 in RAW264.7 cells. Only p38 activation was totally abolished by a blocking anti-RANKL antibody or an excess of RANKL. Surface plasmon resonance experiments revealed that RANK, RANKL and OPG are able to form a tertiary complex. These results suggested a potential formation of a tertiary complex RANK-RANKL-OPG on osteoclasts. Thus, OPG is not only a soluble decoy receptor for RANKL but must be also considered as a direct effector of osteoclast functions.

Animals↗

Only fibres promoting a stable butyrate producing colonic ecosystem decrease the rate of aberrant crypt foci in rats.

BACKGROUND: Dietary fibres have been proposed as protective agents against colon cancer but results of both epidemiological and experimental studies are inconclusive. AIMS: Hypothesising that protection against colon cancer may be restricted to butyrate producing fibres, we investigated the factors needed for long term stable butyrate production and its relation to susceptibility to colon cancer. METHODS: A two part randomised blinded study in rats, mimicking a prospective study in humans, was performed using a low fibre control diet (CD) and three high fibre diets: starch free wheat bran (WB), type III resistant starch (RS), and short chain fructo-oligosaccharides (FOS). Using a randomised block design, 96 inbred rats were fed for two, 16, 30, or 44 days to determine the period of adaptation to the diets, fermentation profiles, and effects on the colon, including mucosal proliferation on day 44. Subsequently, 36 rats fed the same diets for 44 days were injected with azoxymethane and checked for aberrant crypt foci 30 days later. RESULTS: After fermentation had stabilised (44 days), only RS and FOS produced large amounts of butyrate, with a trophic effect in the large intestine. No difference in mucosal proliferation between the diets was noted at this time. In the subsequent experiment one month later, fewer aberrant crypt foci were present in rats fed high butyrate producing diets (RS, p=0.022; FOS, p=0.043). CONCLUSION: A stable butyrate producing colonic ecosystem related to selected fibres appears to be less conducive to colon carcinogenesis.

Animals↗

Differentiation of mucous neck cells into parietal cells: a new concept of mitochondrial biogenesis.

Parietal cells of the gastric fundic mucosa are small and contain only a few tiny mitochondria when they begin to differentiate from mucous neck cells. The canalicular ATPase activity characteristic of mature parietal cells is discrete in these young cells, whereas areas of very high activity are apparent in the Golgi complex, reticulum, nuclear envelope, mitochondrial wall, and plasma membrane. Close relations and contacts occur between mitochondria and these organelles, and the size and number of mitochondria increase progressively. These relations, as well as mitochondrial ATPase activity (a true differentiation marker), cease once the mitochondria become as numerous and large as those of a mature parietal cell. Our observations suggest that a secondary form of mitochondrial biogenesis, involving the massive participation of other organelles and independent of the classical mechanisms inherent in mitosis, occurs in parietal cells at the beginning of G1 phase during the 6 days of their maturation.

4-Nitrophenylphosphatase↗

Electron microscopy study of intrahepatic ultrasmall superparamagnetic iron oxide kinetics in the rat. Relation with magnetic resonance imaging.

Ultrasmall superparamagnetic iron oxide (USPIO) contrast agents for use in magnetic resonance imaging (MRI) are currently undergoing clinical evaluation. However, the images observed and the kinetic profiles obtained differ from one agent to another. In this study, BD IX rats received an intravenous penis injection of the USPIO contrast agents AMI-HS and AMI-227. A cytologic study of the liver was performed, and the data obtained were compared with those of MRI. Images acquired in light microscopy, transmission electron microscopy, microanalysis and electron diffraction provided data on the cell categories involved in the processing of these contrast agents, the importance and modalities of each category relative to this processing, and the modalities of agent elimination. AMI-HS was rapidly removed from the bloodstream by Kupffer's cells and hepatocytes and then eliminated through bile ducts. AMI-227 remained much longer in the blood compartment since it was processed very slowly by endothelial and Kuppfer's cells in the near absence of hepatocytic participation and thus of elimination by the bile ducts. These results allowed us to base our interpretation of MRI sequences on cytologic observations.

Animals↗

Ultrastructural study of degradation of calcium phosphate ceramic by human monocytes and modulation of this activity by HILDA/LIF cytokine.

Biodegradation of ceramics in vivo is achieved essentially by monocytes and multinuclear cells (osteoclasts). Monocytes are the key element in this process because they intervene first at the biomaterial implantation site during inflammatory reaction. In this work, in vitro studies were conducted on an ultrastructural scale to determine the specific behavior of these cells with regard to a calcium phosphate (CaP) ceramic. Two types of phagocytosis were observed when cells came into contact with the biomaterial: either CaP crystals were taken up alone and then dissolved in the cytoplasm after disappearance of the phagosome membrane or they were incorporated together with large quantities of culture medium, in which case dissolution occurred after the formation of heterophagosomes. Phagocytosis of CaP coincided with autophagy and the accumulation of residual bodies in the cells. Addition of HILDA/LIF factor to these cultures induced a very marked decrease in phagocytotic activity directed at the capture of CaP crystals and culture medium. Autophagy was reduced, and residual bodies were rare or absent. This study specifies the role of monocytes in CaP biodegradation and demonstrates for the first time that HILDA/LIF has a biological effect on this cell line.

Animals↗

Effects of interferon gamma (IFN gamma) and tumor necrosis factor alpha (TNF alpha) association in intraperitoneal radioimmunotherapy: studies on an in vitro micrometastasis model.

We considered the usefulness of an association of two cytokines interferon gamma (INF gamma) and tumor necrosis factor alpha (TNF alpha) in optimizing intraperitoneal (i.p.) radioimmunotherapy of ovarian cancer. Studies were performed in conditions similar to those observed in vivo, using tumor multicell spheroids of the SHIN-3 ovarian adenocarcinoma line which expresses CA125 and O3 antigens. Light and electron microscopy showed that this cytokine association caused considerable modification of the three-dimensional morphology of the spheroids and the cells composing them. The uptake and retention kinetics of 125I-labeled F(ab')2 fragments of OC125 and OVTL-3 antibodies indicated that the presence of the cytokines led to a 1.5-fold increase in the quantity of O3 antigen at the spheroid surface. These results were confirmed by autoradiographs showing that the INF gamma-TNF alpha association produced extensive direct antitumor action, with better penetration and uptake of OVTL-3 antibody. Thus, i.p. radioimmunotherapy of micrometastases could be optimized by an initial injection of the IFN gamma-TNF alpha combination.

Antibodies, Monoclonal↗