Literatura académica sobre el tema "Peptide mimétique"
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Artículos de revistas sobre el tema "Peptide mimétique"
Jandrot-Perrus, M., L. Sarda, J. Muzard, S. Loyau, A. Meulemans, L. Louedec, F. Hervatin, J. B. Michel, D. Le Guludec y P. Billiald. "A031 Développement d’un peptido-mimétique de la glycorpotein VI plaquettaire comme outil d’imagerie de la fibrose". Archives of Cardiovascular Diseases 102 (marzo de 2009): S17—S18. http://dx.doi.org/10.1016/s1875-2136(09)72164-3.
Texto completoJacotot, Étienne. "Inhibition des caspases". médecine/sciences 36, n.º 12 (diciembre de 2020): 1143–54. http://dx.doi.org/10.1051/medsci/2020222.
Texto completoRavel, Jean-Marie y Emmanuel J. M. Mignot. "Narcolepsie : une maladie auto-immune affectant un peptide de l’éveil liée à un mimétisme moléculaire avec des épitopes du virus de la grippe". Biologie Aujourd’hui 213, n.º 3-4 (2019): 87–108. http://dx.doi.org/10.1051/jbio/2019026.
Texto completoTesis sobre el tema "Peptide mimétique"
Medali, Tania. "Effet bénéfique de la thiorédoxine et de son peptide mimétique dans l'insuffisance cardiaque". Electronic Thesis or Diss., Sorbonne université, 2023. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2023SORUS198v2.pdf.
Texto completoHeart failure is one of the most devastating human diseases. It is mainly caused by myocardial infarction (MI) which induces obstruction of the coronary artery and loss of the cardiomyocytes. Although limited renewal of cardiomyocytes takes place in the adult heart, it is not sufficient for the regeneration of the contractile function. In contrast, in the postnatal stage, it has been shown that the heart is able to regenerate after injury for 7 days through cardiomyocyte proliferation. At birth, the neonate is exposed to an O2-rich environment, which allows cardiomyocytes to switch from glycolysis to mitochondrial oxidative phosphorylation. This metabolic shift causes an increase in the production of mitochondrial reactive oxygen species (ROS), leading to oxidative changes in proteins and lipids and damage to DNA. These alterations result in cell cycle arrest. However, cell cycle arrest can be reversed in hypoxia or by the action of antioxidants capable of neutralizing the effects of ROS. Among the antioxidant systems, thioredoxins (Trx) are a powerful defense system against ROS. Trx-1 (12 kDa), ubiquitous and highly conserved in all species, is localized in the cytoplasm but can be translocated into the nucleus or secreted extracellularly. In addition to its antioxidant properties, Trx-1 also plays an anti-inflammatory and anti-apoptotic role. Under the action of two α-secretases (ADAM-10 and ADAM-17), Trx-1 is cleaved at its C-terminus to generate a truncated protein called Trx-80. In contrast to Trx-1, Trx-80 lacks oxidative-reducing activity and exerts potent pro-inflammatory and pro-atherogenic effects. Trx-2, localized exclusively in the mitochondria, plays a key role in the detoxification of mitochondrial ROS. Since Trx-1 is cleaved to Trx-80, the use of peptides mimicking its active site thus becomes interesting to evaluate its role in myocardial infarction and bypass the cleavage. Therefore, we used a synthesized mimetic peptide called CB3. This thesis work shows for the first time that CB3 peptide has beneficial effects after MI by improving cardiac functions through cardiac remodeling and cardiac improvement contractility. CB3 is also able to reduce fibrosis, oxidative stress, apoptosis and inflammation which are processes involved in MI. It also induces cell cycle entry and proliferation of cardiomyocytes. These results suggest that CB3 could be a promising therapeutic molecule for MI and heart failure treatment
Rolland, Amandine. "Migration cellulaire : conception, synthèse et évaluation d'analogues synthétiques du peptide PR-21, mimétique de PSA". Thesis, Aix-Marseille 2, 2010. http://www.theses.fr/2010AIX22049.
Texto completoCell migration is a complex process. During development, it contributes to cell reaching their final target. during adulthood, cell migration is involved in immune response or pathological processes.Migration is modulated by adhesion molecules. We concentrated on the Neural Cellular Adhesion Molecule (NCAM) which action is regulated by the post traductional addition of polysialic acid (PSA). PR-21 is a mimetic peptide of PSA-NCAM. In previous studies, PR-21 has been shown to stimulate in the migration of meuroblasts from sub-ventricular zone (SVZ) to the olfactory bulb.We designed non-peptidic analogues of PR-21 on the basis of structural analogies. these analogues were tested on various cell migration models : SVZ explants and C6 over-expressing PSA. We then established the need of key structural functions to modulate cell migration
Rolland, Amandine. "Migration cellulaire : conception, synthèse et évaluation d'analogues synthétiques du peptide PR-21, mimétique de PSA". Electronic Thesis or Diss., Aix-Marseille 2, 2010. http://www.theses.fr/2010AIX22049.
Texto completoCell migration is a complex process. During development, it contributes to cell reaching their final target. during adulthood, cell migration is involved in immune response or pathological processes.Migration is modulated by adhesion molecules. We concentrated on the Neural Cellular Adhesion Molecule (NCAM) which action is regulated by the post traductional addition of polysialic acid (PSA). PR-21 is a mimetic peptide of PSA-NCAM. In previous studies, PR-21 has been shown to stimulate in the migration of meuroblasts from sub-ventricular zone (SVZ) to the olfactory bulb.We designed non-peptidic analogues of PR-21 on the basis of structural analogies. these analogues were tested on various cell migration models : SVZ explants and C6 over-expressing PSA. We then established the need of key structural functions to modulate cell migration
Smith, Rémy. "Caractérisation d'un nouveau modèle de vieillissement de macrophages in vitro et évaluation de l'efficacité thérapeutique d'un peptide mimétique de la thiorédoxine-1". Electronic Thesis or Diss., Sorbonne université, 2023. http://www.theses.fr/2023SORUS727.
Texto completoDuring aging, a low-grade chronic inflammation develops at the cellular, tissue, and circulating levels, known as inflamm'aging. It is defined as an imbalance between pro- and anti-inflammatory processes and is considered as a common etiological mechanism for age-related pathologies. Inflamm'aging is primarily attributed to immune response alterations (immunosenescence) and the accumulation of senescent cells (SC) in aged tissues. SC are characterized by cell cycle arrest (p16INK4a and p21CIP induction) and the expression of senescence markers such as SA-β-Gal (senescence-associated β-galactosidase activity). SC also adopt a senescence-associated secretory phenotype (SASP) and produce pro-inflammatory cytokines (IL-6, IL-1β, MCP-1...), thus contributing to inflamm'aging establishment. The accumulation of SC leads to chronic activation of innate immune cells, particularly macrophages. Macrophages are highly phenotypically plastic cells that can adapt their physiology based on the tissue microenvironment. Recent studies have described that macrophages undergo phenotypic adaptation in the SC-rich tissue microenvironment, adopting a senescent-like phenotype characterized by high expression of p16Ink4a, SA-β-Gal, and inflammation markers. Aged macrophages also exhibit metabolic alterations corresponding to a pro-inflammatory metabolic phenotype, including increased glycolysis. Furthermore, they have reduced capacity to respond to inflammatory signals and carry out phagocytic activity, leading to the accumulation of senescent cells and chronic inflammation. Limiting the accumulation of senescent cells and associated inflamm'aging is a major challenge in preventing age-related pathologies. One potential therapeutic strategy involves the use of senomorphic molecules to modulate the SASP of SC and mitigate inflamm'aging. In this context, we are particularly interested in thioredoxin-1 (Trx-1). Trx-1 is an oxidoreductase that exerts antioxidant and anti-inflammatory effects through its catalytic site (-Cys32-Gly-ProCys35-). However, it can be cleaved, through a mechanism that is still poorly understood, into a truncated form, Trx-80, which exacerbates inflammation. Notably, Trx-80 increases in the plasma of healthy and aged subjects at the expense of Trx-1. Given that, the therapeutic use of Trx-1 during aging is compromised by its cleavage, we have developed a new strategy based on a tripeptide, mimicking the catalytic site of Trx-1 and its effects, called CB3. We have previously demonstrated that CB3 exerts antioxidant and anti-inflammatory effects in a murine model of vascular inflammation. However, the beneficial effects of CB3 in the context of aging remain to be demonstrated. For this purpose, we characterized a new model of macrophage aging in vitro, based on comparing a normal culture (day 2) with prolonged cultures (7 and 14 days) of peritoneal macrophages derived from 3-month-old mice. The D14 cultures express all previously described markers of senescence and immunosenescence, enabling us to evaluate the therapeutic efficacy of CB3. It is capable of reducing SASP, expression levels of p16INK4a, p21CIP, and reinitiating the cell cycle by increasing EdU incorporation. These results have led to the development of a relevant model for studying the altered functions and characteristics of macrophages during aging, as well as a new therapeutic approach to counteract senescence and inflamm'aging
Canesi, Fanny. "Les peptides mimétiques de la Thiorédoxine-1 : nouvelle stratégie thérapeutique pour les maladies cardiovasculaires". Thesis, Sorbonne université, 2018. http://www.theses.fr/2018SORUS500.
Texto completoOxidative stress and inflammation play a pathogenic role in atherosclerosis. Thioredoxin-1 (Trx-1) is an anti-oxidative, anti-inflammatory protein with atheroprotective effects. However, in vivo cleavage of Trx-1 generates a truncated pro-inflammatory protein, Trx-80, which compromises the therapeutic use of Trx-1. The aim of my thesis is to characterize a new therapeutic strategy based on Trx-mimetic peptides (TxMP) for the treatment of atherosclerosis. We synthesized a small peptide based on the active site of Trx-1 named CB3. Firstly, CB3 was validated on cultured peritoneal murine macrophages (cellular viability, anti-oxidant and anti-inflammatory responses). Secondly, the atherosclerotic mouse model (ApoE2.Ki) fed a high fat diet was intraperitoneally injected with CB3 to measure their anti-oxidant, anti-inflammatory and anti-atherogenic effects. Our results clearly showed that, similar to the full length Trx-1, CB3 exerts protective effects by reducing inflammation and oxidative stress in macrophages and in ApoE.Ki mice. The atheroprotective effect of CB3 opens promising therapeutic approaches for treatment of atherosclerosis
Peter, Jean-Christophe. "Des peptides et peptido-mimétiques ligands de récepteurs cardio-vasculaires". Université Louis Pasteur (Strasbourg) (1971-2008), 2004. http://www.theses.fr/2004STR13093.
Texto completoG protein coupled receptor are involved in various metabolic functions. This receptor family represents the main target of cardiovascular and neurological used drugs. The 2 adrenergic receptor (2AR) and the M2 muscarinic receptor (M2Ach-R) belong to this family and are implicated in the regulation of the cardiovascular system. Many studies show the importance of the second extracellular loop of GPCR on their activity in particular in some autoimmune diseases. The first part of this work concern the 2AR. Using a functional monoclonal antibody against the human 2AR, a scFv fragment with high affinity for the target epitope was constructed and produced. The fragment recognized the ß2-adrenergic receptors on A431 cells, blocked cAMP accumulation induced by the ß2-agonist salbutamol, and decreased basal cAMP accumulation in the same cells. Their in vitro activity was tested on neonatal rat cardiomyocytes. The antibody fragments blocked the chronotropic activity induced by the ß2-agonist clenbuterol. They also decreased the in vivo heart beating frequency of mice pretreated with bisoprolol (a ß1-adrenergic receptor antagonist) for 4 minutes after injection. Cyclic peptides derived from the CDR of the scFv 6H8 were produced. The CDR H1 was not used because of its total insolubility in water. Kinetic contants of interaction with their target peptides were determined by SPR technology for the CDR peptides L2, L3 and H3. The CDR H2, L1 et L2 behaved as negative allosteric modulator of the 2AR, they inhibited in a non competitive manner the increase of spontaneous beating rate of neonatal rat cardiomyocytes induced by an increasing dose of clenbuterol. The CDR H3 and L3 behaved as positive allosteric modulators of the 2AR by increasing the clenbuterol effect on these cells. The second part of this work concern the modulation of the M2Ach-R activity using two different strategies. First, we investigated the in vivo consequences on heart rate of such antibodies in mice immunized with a peptide derived from the second extracellular loop of the M2AChR. Nine mice, immunized with a peptide corresponding to the N-terminus of the second extracellular loop of the M2AChR were compared to 9 mice immunized with an irrelevant peptide. Sera of mice immunized with the M2ACh-R derived peptide recognized the M2ACh-R on immunoblots and enhanced the agonist activity of carbachol towards the M2AChR transfected in CHO cells. In vivo, no difference could be shown in heart rate nor in heart rate variability between the two groups of mice. In contrast, the decrease in heart rate induced by carbachol was more pronounced in the M2AChR immunized mice compared to the control mice. The increase in heart rate induced by atropine, gallamine and isoproterenol were alike significantly attenuated in the M2ACh-R immunized mice compared to the control mice. Analysis of heart rate variability further argued for an increased parasympathetic response to the different drugs in the M2ACh-R immunized mice. Antibodies raised against the M2AChR can behave as positive M2AchR allosteric modulators in vivo. They might be protective in boosting the activity of the parasympathetic drive to the heart, in particular in patients with a high sympathetic tone. The second strategy was, to construct and produce a single chain variable fragment, from a partial agonist monoclonal antibody directed against the M2ACh-R. It showed high affinity for its target epitope. The fragment is able to recognize its receptor on Chinese hamster ovary cells transfected with the M2ACh-R, to block the effect of carbachol on this receptor and to exert an inverse agonist activity on the basal activity of the receptor. The antibody fragment is also able to increase the basal rhythm of cultured neonatal rat cardiomyocytes, and to inhibit in a non-competitive manner the negative chronotropic effect of carbachol. This antibody fragment is able to exert its inverse agonist activity in vivo on mice heart activity. This works shows that recombinant monovalent antibody fragments directed against te second extracellular loop of GPCR have inverse agonist activity. Bivalent antibodies directed against the same target, show an allosteric positive activity on the receptor. Peptides derived from CDR of the scFv 6H8, keep a pharmacological function, they act as allosteric modulators of the 2AR. These scFv and cyclic peptides may represent leads for a new class of allosteric modulators of GPCR. They also represent tools for understanding of the activation mechanisms of GPCR
Ma, Xin. "Synthèse de mimétiques de gamma-"turns"". Montpellier 2, 1994. http://www.theses.fr/1994MON20029.
Texto completoMuzard, Julien. "Glycoprotéine VI plaquettaire : développement d'un fragment d'anticorps recombinant anti-thrombotique et d'un peptido-mimétique". Paris 7, 2007. http://www.theses.fr/2007PA077174.
Texto completoGlycoprotein VI (GPVI), the major receptor for platelet activation by collagens, plays an important role in arterial thrombosis, a pathologic process common to cardiovascular diseases. Inhibition of GPVI-collagen interaction could represent an attractive strategy to develop antithrombotic molecules. Two approaches were evaluated in this study : 1) Blocking GPVI with a recombinant antibody fragment, and 2) Using a soluble peptidomimetick witch compete with GPVI for binding to collagen. Strategy 1 : Starting from 9O12. 2 hybridoma secreting a monoclonal IgG, a recombinant single chain antibody fragment was design and expressed as a recombinant protein in the periplasm of bacteria. It retains the binding proprietes of the parental IgG (high affinity, neutralisation of GPVI-collagen interaction). Purified scFv is able to inhibit platelet aggregation induced by collagen in vitro in conditions which mimick the arterial flow. The humanized scFv were next obtained an it can be use as a starting block to design a recombinant therapeutic humanized Fab fragment. Strategy 2 : After screening of a random dodecapeptide library expressed at the bacterial surface with the neutralizing antibody IgG 9O12. 2, solubles peptidomimeticks of human GPVI were identified. One of them were synthetized as constrained peptide. It binds to collagen, compete with GPVI for binding to collagen (KD=10"8M). Fibrosis (collagen accumulation) was detected in vivo using radiolabelled peptide. This capacity to bind to collagen is used to develop an non invasive isotopic imagery method for the diagnostic and the evolution of fibrosis
Andriuzzi, Olivia. "Vers de nouveaux inhibiteurs de glycosidases de type glyco- ou peptido- mimétique : synthèse et évaluation biologique". Paris 5, 2004. http://www.theses.fr/2004PA05P630.
Texto completoConception of glycosidases inhibitors is a task of major interest in therapeutical chemistry. The purpose of this thesis was the synthesis and the biological evaluation of potential inhibitors : Glycomimetic inhibitors, mimicking the substrate or its transition state within the active site. Access to cyclooctanic carbasugars and aminocyclitols from D-mannitol bis-epoxides involves a key step of carbacyclisation by ring closing metathesis or by pinacolic coupling. Peptidomimetic inhibitors, mimicking tendamistat's b turn, powerfull inhibitor of a-amylase. Access to the 1,4-diazepan-2-one scaffold involves two key intermediates : an amino-epoxyde, obtained from D-iso ou L-ascorbic acid and an amino acid. The two key steps are : the opening of the epoxide by the amine functionnality of the aminoacide and the peptidic coupling between the carboxylic acid of the aminoacid and the amine functionality of the amino-epoxyde
Granier, Sébastien. "Interaction des récepteurs de la vasopressine avec leurs partenaires intracellulaires : Approche peptido-mimétique, pharmacologique et protéomique". Montpellier 2, 2004. http://www.theses.fr/2004MON20152.
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