7 results on '"Monfoulet L"'
Search Results
2. Strategies for improving the efficacy of bioengineered bone constructs: a perspective
- Author
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Petite, H., Vandamme, K., Monfoulet, L., and Logeart-Avramoglou, D.
- Published
- 2011
- Full Text
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3. An update on the role of nutrigenomic modulations in mediating the cardiovascular protective effect of fruit polyphenols.
- Author
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Krga I, Milenkovic D, Morand C, and Monfoulet LE
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- Animals, Cell Line, Diet, Flavanones, Flavonoids, Gene Expression, Health Promotion, Human Umbilical Vein Endothelial Cells, Humans, Cardiovascular Diseases prevention & control, Fruit chemistry, Nutrigenomics, Polyphenols administration & dosage
- Abstract
Polyphenols are plant food microconstituents that are widely distributed in the human diet, with fruits and fruit-derived products as one of the main dietary sources. Epidemiological studies have shown an inverse relationship between the intake of different classes of polyphenols and the risk of myocardial infarction or cardiovascular disease (CVD) mortality. These compounds have been associated with the promotion of cardiovascular health as evidenced by clinical studies reporting beneficial effects of polyphenol-rich fruit consumption on intermediate markers of cardiovascular diseases. Additionally, animal and in vitro studies have indicated positive roles of polyphenols in preventing dysfunctions associated with the development of cardiovascular diseases. However, the mechanisms of action underlying their beneficial effects appear complex and are not fully understood. This review aims to provide an update on the nutrigenomic effects of different groups of polyphenols from fruits and especially focuses on their cardiovascular protective effects in cell and animal studies.
- Published
- 2016
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- View/download PDF
4. Bone sialoprotein, but not osteopontin, deficiency impairs the mineralization of regenerating bone during cortical defect healing.
- Author
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Monfoulet L, Malaval L, Aubin JE, Rittling SR, Gadeau AP, Fricain JC, and Chassande O
- Subjects
- Animals, Diaphyses diagnostic imaging, Diaphyses pathology, Diaphyses physiopathology, Femur diagnostic imaging, Femur physiopathology, Femur surgery, Gene Expression Regulation, Integrin-Binding Sialoprotein, Mice, Osteogenesis physiology, Osteopontin genetics, Osteopontin metabolism, Sialoglycoproteins genetics, Sialoglycoproteins metabolism, Wound Healing genetics, X-Ray Microtomography, Bone Regeneration physiology, Calcification, Physiologic physiology, Femur pathology, Osteopontin deficiency, Sialoglycoproteins deficiency, Wound Healing physiology
- Abstract
Bone healing is a complex multi-step process, which depends on the position and size of the lesion, and on the mechanical stability of the wounded area. To address more specifically the mechanisms involved in cortical bone healing, we created drill-hole defects in the cortex of mouse femur, a lesion that triggers intramembranous repair, and compared the roles of bone sialoprotein (BSP) and osteopontin (OPN), two proteins of the extracellular matrix, in the repair process. Bone regeneration was analyzed by ex vivo microcomputerized X-ray tomography and histomorphometry of bones of BSP-deficient, OPN-deficient and wild-type mice. In all mouse strains, the cortical gap was bridged with woven bone within 2 weeks and no mineralized tissue was observed in the marrow. Within 3 weeks, lamellar cortical bone filled the gap. The amount and degree of mineralization of the woven bone was not affected by OPN deficiency, but cortical bone healing was delayed in BSP-deficient mice due to delayed mineralization. Gene expression studies showed a higher amount of BSP transcripts in the repair bone of OPN-deficient mice, suggesting a possible compensation of OPN function by BSP in OPN-null mice. Our data suggest that BSP, but not OPN, plays a role in primary bone formation and mineralization of newly formed bone during the process of cortical bone healing., ((c) 2009 Elsevier Inc. All rights reserved.)
- Published
- 2010
- Full Text
- View/download PDF
5. Drilled hole defects in mouse femur as models of intramembranous cortical and cancellous bone regeneration.
- Author
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Monfoulet L, Rabier B, Chassande O, and Fricain JC
- Subjects
- Animals, Diaphyses injuries, Diaphyses physiology, Diaphyses surgery, Disease Models, Animal, Epiphyses injuries, Epiphyses physiology, Epiphyses surgery, Femur injuries, Male, Mice, Mice, Inbred C57BL, Microsurgery methods, Orthopedic Procedures methods, Reproducibility of Results, Species Specificity, X-Ray Microtomography, Bone Regeneration physiology, Femur physiology, Femur surgery, Wound Healing physiology
- Abstract
In order to identify pertinent models of cortical and cancellous bone regeneration, we compared the kinetics and patterns of bone healing in mouse femur using two defect protocols. The first protocol consisted of a 0.9-mm-diameter through-and-through cortical hole drilled in the mid-diaphysis. The second protocol was a 0.9-mm-diameter, 1-mm-deep perforation in the distal epimetaphyseal region, which destroyed part of the growth plate and cancellous bone. Bone healing was analyzed by ex vivo micro-computerized X-ray tomography and histology. In the diaphysis, the cortical gap was bridged with woven bone within 2 weeks. This newly formed bone was rapidly remodeled into compact cortical bone, which showed characteristic parameters of intact cortex 4 weeks after surgery. In the epimetaphysis, bone formation was initiated at the deepest region of the defect and spread slowly toward the cortical gap. In this position, newly formed bone quickly adopted the characteristics of trabecular bone, whereas a thin compact wall was formed at its external border, which reached the density of intact cortical bone but failed to bridge the cortical gap even 13 weeks after surgery. This comparative study indicates that the diaphyseal defect is a model of cortical bone healing and that the epimetaphyseal defect is a model of cancellous bone repair. These models enable experimental genetics studies to investigate the cellular and molecular mechanisms of spontaneous cortical and cancellous bone repair and may be useful for pharmacological studies.
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- 2010
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6. Absence of ERRalpha in female mice confers resistance to bone loss induced by age or estrogen-deficiency.
- Author
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Teyssier C, Gallet M, Rabier B, Monfoulet L, Dine J, Macari C, Espallergues J, Horard B, Giguère V, Cohen-Solal M, Chassande O, and Vanacker JM
- Subjects
- Aging, Animals, Bone Marrow metabolism, Bone and Bones pathology, Cell Differentiation, Cell Line, Estrogen Receptor alpha metabolism, Female, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Tomography, X-Ray Computed methods, Bone and Bones metabolism, Estrogen Receptor alpha genetics, Estrogens metabolism, Osteopontin metabolism
- Abstract
Background: ERRalpha is an orphan member of the nuclear hormone receptor superfamily, which acts as a transcription factor and is involved in various metabolic processes. ERRalpha is also highly expressed in ossification zones during mouse development as well as in human bones and cell lines. Previous data have shown that this receptor up-modulates the expression of osteopontin, which acts as an inhibitor of bone mineralization and whose absence results in resistance to ovariectomy-induced bone loss. Altogether this suggests that ERRalpha may negatively regulate bone mass and could impact on bone fragility that occurs in the absence of estrogens., Methods/principal Findings: In this report, we have determined the in vivo effect of ERRalpha on bone, using knock-out mice. Relative to wild type animals, female ERRalphaKO bones do not age and are resistant to bone loss induced by estrogen-withdrawal. Strikingly male ERRalphaKO mice are indistinguishable from their wild type counterparts, both at the unchallenged or gonadectomized state. Using primary cell cultures originating from ERRalphaKO bone marrow, we also show that ERRalpha acts as an inhibitor of osteoblast differentiation., Conclusion/significance: Down-regulating ERRalpha could thus be beneficial against osteoporosis.
- Published
- 2009
- Full Text
- View/download PDF
7. Absence of bone sialoprotein (BSP) impairs cortical defect repair in mouse long bone.
- Author
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Malaval L, Monfoulet L, Fabre T, Pothuaud L, Bareille R, Miraux S, Thiaudiere E, Raffard G, Franconi JM, Lafage-Proust MH, Aubin JE, Vico L, and Amédée J
- Subjects
- Animals, Bone Remodeling, Bone and Bones diagnostic imaging, Bone and Bones surgery, Integrin-Binding Sialoprotein, Magnetic Resonance Imaging, Mice, Sialoglycoproteins metabolism, X-Ray Microtomography, Bone and Bones pathology, Sialoglycoproteins deficiency, Wound Healing
- Abstract
Matrix proteins of the SIBLING family interact with bone cells and with bone mineral and are thus in a key position to regulate bone development, remodeling and repair. Within this family, bone sialoprotein (BSP) is highly expressed by osteoblasts, hypertrophic chondrocytes and osteoclasts. We recently reported that mice lacking BSP (BSP-/-) have very low trabecular bone turnover. In the present study, we set up an experimental model of bone repair by drilling a 1 mm diameter hole in the cortical bone of femurs in both BSP-/- and +/+ mice. A non-invasive MRI imaging and bone quantification procedure was designed to follow bone regeneration, and these data were extended by microCT imaging and histomorphometry on undecalcified sections for analysis at cellular level. These combined approaches revealed that the repair process as reflected in defect-refilling in the cortical area was significantly delayed in BSP-/- mice compared to +/+ mice. Concomitantly, histomorphometry showed that formation, mineralization and remodeling of repair (primary) bone in the medulla were delayed in BSP-/- mice, with lower osteoid and osteoclast surfaces at day 15. In conclusion, the absence of BSP delays bone repair at least in part by impairing both new bone formation and osteoclast activity.
- Published
- 2009
- Full Text
- View/download PDF
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