Propriétés rhéologiques de farines panifiables formulées à partir d’extraits d’amidon et de gluten de blé

Le présent travail a mis en évidence les propriétés rhéologiques des farines panifiables reconstituées avec des extraits d’amidon. Du gluten vital 10% a été incorporé à 90% d’extraits d’amidons de blé, de maïs,de riz et de la pomme de terre pour obtenir, respectivement, quatre (4) types de farines F1, F2, F3 et F4. Les farines ont été reconstituées à l’aide d’un mélangeur de type KENWOOD à 4 unités de vitesse. Les caractéristiques rhéologiques des pâtes des farines reconstituées ont été analysées à l’aide du Farinographe Brabender et de l’Alvéographe Chopin. Les farines F2, F3 et F4 sont caractérisées par une forte capacité d’hydratation, une faible activité a-amylasique qui se traduit par des temps de chute très élevés. Il en résulte des pâtes de très faible tenue avec une résistance à l’extraction, en comparaison avec une farine de référence (Fo). La force de la pâte de la farine F1 est plus élevée (W = 85.10-4 J) que celle des pâtes des farines F2, F3 et F4. Globalement, l’équilibre de configuration (P/L) entre la ténacité et l’élasticité des pâtes des farines est de l’ordre de 0,88 alors que les indices d’élasticité varient entre 7,3 et 9,4

Structure de l'amidon de maïs et principaux phénomènes impliqués dans sa modification thermique

Structures and phenomena occurring during the heat treatment of cornstarch. The structure of cornstarch and the modifications induced during the heat treatments are presented in this review. Current knowledge indicate that the starch granules are semi-crystalline entities composed mainly by amylose and amylopectin, undergoing deep reorganizations during the heat treatments. Gelatinization, glass transitions, relaxation phenomena, retrogradation and the formation of amylose-lipids complexes are the major phenomena involved in these reorganisations, and are the basis of changes of the techno-functional properties of cornstarch-based products during their heat treatment. La rhizosphère est le volume du sol situé au voisinage immédiat des racines des plantes et qui se caractérise par la présence d'exsudats racinaires (rhizodépôts). Ces exsudats sont utilisés par la microflore endémique en tant que signaux chimiques en plus d'être un substrat nutritif disponible pour la croissance et le développement de ces microorganismes dans la rhizosphère. Certaines de ces bactéries du sol, appelées PGPRs (Plant Growth Promoting Rhizobacteria), sont capables de coloniser les racines ou bien encore la rhizosphère, mais à la différence des autres bactéries rhizosphériques elles ont, en retour, un effet bénéfique sur la plante. Cet effet bénéfique peut être direct, ou indirect. La promotion directe de la croissance est le résultat du pouvoir d'acquisition des nutriments ou de la stimulation des hormones de la plante. D'autres mécanismes indirects, mais le plus souvent liés à la croissance des plantes, sont impliqués dans la réduction/suppression des pathogènes des plantes. Cet article décrit les différents mécanismes mis en jeu par les PGPRs dans leur environnement naturel pour influencer favorablement la croissance et la santé des plantes

MMP-9 regulates both positively and negatively collagen gel contraction - A nonproteolytic function of MMP-9

peer reviewedaudience: researcher, professionalObjective: Constrictive remodeling accounts for lumen loss in postangioplasty restenosis. Matrix metalloproteinase-9 (MMP-9) has been shown to prevent constrictive remodeling in vivo. To investigate potential mechanisms for this observation, we investigated the role of MMP-9 in smooth muscle cell (SMC)-mediated collagen gel contraction, an in vitro model of constrictive remodeling. Methods: Fischer rat SMCs were stably transfected with a construct-expressing rat-MMP-9 under the control of a tetracycline (Tet)-off promoter. SMCs were seeded in type 1 collagen gels (2.4 mg/ml) in the presence or not of tetracycline (1 mu g/ml), and gel contraction was defined as the percentage of retraction of the collagen gel. The depletion of MMP-9 was obtained by using siRNA targeting MMP-9 mRNA or a blocking antibody. Results: Gel contraction was significantly reduced at all times when MMP-9 was overexpressed (Tet-) as compared with the control condition (Tet+). However, MMP-9 depletion of control (Tet+) SMCS (using siRNA or antibody) also inhibited gel contraction. To resolve the apparent discrepancy and determine if MMP-9 exerts a dose-dependent biphasic effect on gel contraction, conditioned medium and purified rat-MMP-9 were prepared. Gel contraction was significantly increased by addition of 0.8 mg/ml of MMP-9, while high concentrations of MMP-9 (>= 100 mg/ml) inhibited contraction. The addition of BB94 and TIMP-1 did not alter the inhibitory or stimulatory effect of MMP-9. Conclusions: Our data Suggest that MMP-9, independent of its proteolytic function, has a biphasic effect on SMC-mediated collagen gel contraction. Understanding the different roles of MMP-9 Should allow the development of better therapeutic strategies for restenotic vascular disease. (c) 2004 European Society of Cardiology. Published by Elsevier B.V. All rights reserved

Newly identified biologically active and proteolysis-resistant VEGF-A isoform VEGF111 is induced by genotoxic agents

Ultraviolet B and genotoxic drugs induce the expression of a vascular endothelial growth factor A (VEGF-A) splice variant (VEGF111) encoded by exons 1–4 and 8 in many cultured cells. Although not detected in a series of normal human and mouse tissue, VEGF111 expression is induced in MCF-7 xenografts in nude mice upon treatment by camptothecin. The skipping of exons that contain proteolytic cleavage sites and extracellular matrix–binding domains makes VEGF111 diffusible and resistant to proteolysis. Recombinant VEGF111 activates VEGF receptor 2 (VEGF-R2) and extracellularly regulated kinase 1/2 in human umbilical vascular endothelial cells and porcine aortic endothelial cells expressing VEGF-R2. The mitogenic and chemotactic activity and VEGF111's ability to promote vascular network formation during embyonic stem cell differentiation are similar to those of VEGF121 and 165. Tumors in nude mice formed by HEK293 cells expressing VEGF111 develop a more widespread network of numerous small vessels in the peritumoral tissue than those expressing other isoforms. Its potent angiogenic activity and remarkable resistance to proteolysis makes VEGF111 a potential adverse factor during chemotherapy but a beneficial therapeutic tool for ischemic diseases

Progression in MCF-7 Breast Cancer Cell Tumorigenicity: Compared Effect of FGF-3 and FGF-4.

The transforming properties of fibroblast growth factor 3 (FGF-3) were investigated in MCF7 breast cancer cells and compared to those of FGF-4, a known oncogenic product. The short form of fgf-3 and the fgf-4 sequences were each introduced with retroviral vectors and the proteins were only detected in the cytoplasm of the infected cells, as expected. In vitro, cells producing FGF-3 (MCF7.fgf-3) and FGF-4 (MCF7.fgf-4) displayed an amount of estrogen receptors decreased to around 45% of the control value. However, MCF7.fgf-3 cell proliferation remained responsive to estradiol supply. The sensitivity of the MCF7.fgf-4 cells, if existant, was masked by the important mitogenic action exerted by FGF-4. In vivo, the MCF7.fgf-3 and MCF7.fgf-4 cells gave rise to tumors under conditions in which the control cells were not tumorigenic. Supplementing the mice with estrogen had the paradoxical effect of totally suppressing the start of the FGF-3 as well as the FGF-4 tumors. Tumorigenicity in the presence of matrigel was similar for MCF7.fgf-3 and control cells and was increased by estrogen supplementation. Once started, the MCF7.fgf-4 tumors grew with a characteristic high rate. Remarkably, FGF-4 but not FGF-3, stimulated the secretion of vascular endothelial growth factor (VEGF165) without altering the steady-state level of its mRNA, suggesting a possible regulation of VEGF synthesis at the translational level in MCF7 cells. The increased VEGF secretion is probably involved in the more aggressive phenotype of the MCF7.fgf-4 cells while a decreased dependence upon micro-environmental factors might be part of the increased tumorigenic potential of the MCF7.fgf-3 cells.Peer reviewe

MicroRNA-21 Exhibits Antiangiogenic Function by Targeting RhoB Expression in Endothelial Cells

BACKGROUND: MicroRNAs (miRNAs) are endogenously expressed small non-coding RNAs that regulate gene expression at post-transcriptional level. The recent discovery of the involvement of these RNAs in the control of angiogenesis renders them very attractive in the development of new approaches for restoring the angiogenic balance. Whereas miRNA-21 has been demonstrated to be highly expressed in endothelial cells, the potential function of this miRNA in angiogenesis has never been investigated. METHODOLOGY/PRINCIPAL FINDINGS: We first observed in endothelial cells a negative regulation of miR-21 expression by serum and bFGF, two pro-angiogenic factors. Then using in vitro angiogenic assays, we observed that miR-21 acts as a negative modulator of angiogenesis. miR-21 overexpression reduced endothelial cell proliferation, migration and the ability of these cells to form tubes whereas miR-21 inhibition using a LNA-anti-miR led to opposite effects. Expression of miR-21 in endothelial cells also led to a reduction in the organization of actin into stress fibers, which may explain the decrease in cell migration. Further mechanistic studies showed that miR-21 targets RhoB, as revealed by a decrease in RhoB expression and activity in miR-21 overexpressing cells. RhoB silencing impairs endothelial cell migration and tubulogenesis, thus providing a possible mechanism for miR-21 to inhibit angiogenesis. Finally, the therapeutic potential of miR-21 as an angiogenesis inhibitor was demonstrated in vivo in a mouse model of choroidal neovascularization. CONCLUSIONS/SIGNIFICANCE: Our results identify miR-21 as a new angiogenesis inhibitor and suggest that inhibition of cell migration and tubulogenesis is mediated through repression of RhoB