Docteur SYLVIE FOURNIER

Bibliographie

• Classification of Stevia rebaudiana Chemotypes Based on Steviol Glycosides and Their Identified Malonyl Forms Using Liquid Chromatography Coupled to High-Resolution Mass Spectrometry

  2025

  ArticleJournal of Agricultural and Food Chemistry

• Deciphering transcriptomic and metabolomic wood responses to grapevine trunk diseases-associated fungi

  2024

  ArticlePhytoFrontiers

• Transition to ripening in tomato requires hormone-controlled genetic reprogramming initiated in gel tissue

  2022

  ArticlePlant Physiology

• Environmental filtering and maternal effects on the phenotype of a neotropical bromeliad

  2022

  CongrèsEuropean Conference of TroEuropean Conference of Tropical Ecology - The Future of tropical ecosystems - news insights and innovative methodspical Ecology - The future of tropical ecosystems - new insights and innovative methods

• Modification of Early Response of Vitis vinifera to Pathogens Relating to Esca Disease and Biocontrol Agent Vintec® Revealed By Untargeted Metabolomics on Woody Tissues

  2022

  ArticleFrontiers in Microbiology

• Cannabinoids vs. whole metabolome: Relevance of cannabinomics in analyzing Cannabis varieties

  2021

  ArticleAnalytica Chimica Acta

• Phytohormone production by the arbuscular mycorrhizal fungus Rhizophagus irregularis

  2020

  ArticlePLoS ONE

• MS-CleanR: A Feature-Filtering Workflow for Untargeted LC–MS Based Metabolomics

  2020

  ArticleAnalytical Chemistry

Source : HAL — archive ouverte CCSD/CNRS (couvre articles, chapitres EMC, communications congrès, thèses).

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Top publications · les plus citées

• 1

  The interleukin-1 receptor in normal and osteoarthritic human articular chondrocytes. Identification as the type I receptor and analysis of binding kinetics and biologic function

  Arthritis and rheumatism · 1992

  📚 166 citations🎯 RCR 5.23Top 7% NIH

  Lire l'abstract Crossref ↓

  AbstractObjective. To identify and investigate the kinetic binding properties of interleukin‐1 receptors (IL‐1R), and examine the abilities of the 2 IL‐1 isoforms to stimulate metalloprotease synthesis, in normal and osteoarthritic (OA) chondrocytes.Methods. Receptor affinity and density were determined using radioligand binding experiments and flow cytometry. Immunocytochemical analysis and affinity cross‐linking studies were performed for characterization of IL‐1R.Results. While no difference in receptor affinity between normal and OA chondrocytes was noted in binding studies (kd ˜30 pM), a 2‐fold increase in receptor density was found in OA chondrocytes as compared with normal chondrocytes (mean 4,069 sites/cell versus 2,315 sites/cell). Flow cytometry experiments also showed a significant increase in receptor density in OA cells, as well as an enhancement in the percentage of positive cells in diseased cartilage compared with normal. Binding data for both IL‐1 isoforms revealed a single class of binding sites and receptor specificity. Factors such as IL‐2, interferon‐sγ, tumor necrosis factor α, and bovine insulin did not compete with IL‐1β. By covalent ligand cross‐linking and electrophoretic analysis, only type I IL‐1R, a protein of 80 kd, was detected on chondrocytes. By immunocytochemical analysis, IL‐1R was identified at the cell membrane level, in both normal and OA chondrocytes. The presence of nuclear staining was also observed, but only in OA chondrocytes. Recombinant human IL‐1 (α and β) induced the secretion of stromelysin and collagenase in a dose‐dependent manner. The IL‐1 concentration required for half‐maximal metalloprotease stimulation was 3–4 times lower in OA chondrocytes than in normal cells.Conclusion. These results indicate that OA chondrocytes have a higher sensitivity to the stimulation of metalloprotease synthesis by IL‐1 than do normal cells. This could be related to the increased levels of IL‐1R expressed in the OA cells. The implications of these findings with regard to the possible roles of IL‐1 and IL‐1R in the pathogenesis of OA are discussed.

• 2

  Characterization of relapsing-remitting and chronic forms of experimental autoimmune encephalomyelitis in C57BL/6 mice

  Glia · 2010

  📚 118 citations🎯 RCR 3.00Top 16% NIH

  Lire l'abstract Crossref ↓

  AbstractMultiple sclerosis (MS) is an autoimmune, demyelinating disease of the central nervous system (CNS). Like MS, the animal model experimental autoimmune encephalomyelitis (EAE) is characterized by CNS inflammation and demyelination and can follow a relapsing–remitting (RR) or chronic (CH) disease course. The molecular and pathological differences that underlie these different forms of EAE are not fully understood. We have compared the differences in RR‐ and CH‐EAE generated in the same mouse strain (C57BL/6) using the same antigen. At the peak of disease when mice in both groups have similar clinical scores, CH‐EAE is associated with increased lesion burden, myelin loss, axonal damage, and chemokine/cytokine expression when compared with RR‐EAE. We further showed that inflammation and myelin loss continue to worsen in later stages of CH‐EAE, whereas these features are largely resolved at the equivalent stage in RR‐EAE. Additionally, axonal loss at these later stages is more severe in CH‐EAE than in RR‐EAE. We also demonstrated that CH‐EAE is associated with a greater predominance of CD8+ T cells in the CNS that exhibit MOG35–55 antigen specificity. These studies therefore showed that, as early as the peak stage of disease, RR‐ and CH‐EAE differ remarkably in their immune cell profile, chemokine/cytokine responses, and histopathological features. These data also indicated that this model of CH‐EAE exhibits pathological features of a chronic‐progressive disease profile and suggested that the sustained chronic phenotype is due to a combination of axonal loss, myelin loss, and continuing inflammation. © 2009 Wiley‐Liss, Inc.

• 3

  Arabidopsis wat1 (walls are thin1)-mediated resistance to the bacterial vascular pathogen, Ralstonia solanacearum, is accompanied by cross-regulation of salicylic acid and tryptophan metabolism

  The Plant journal : for cell and molecular biology · 2013

  📚 106 citations🎯 RCR 3.70Top 12% NIH🔓 Open Access📄 PDF gratuit ↗

  Lire l'abstract Crossref ↓

  SummaryInactivation of Arabidopsis WAT1 (Walls Are Thin1), a gene required for secondary cell‐wall deposition, conferred broad‐spectrum resistance to vascular pathogens, including the bacteria Ralstonia solanacearum and Xanthomonas campestris pv. campestris, and the fungi Verticillium dahliae and Verticillium albo‐atrum. Introduction of NahG, the bacterial salicylic acid (SA)‐degrading salicylate hydroxylase gene, into the wat1 mutant restored full susceptibility to both R. solanacearum and X. campestris pv. campestris. Moreover, SA content was constitutively higher in wat1 roots, further supporting a role for SA in wat1‐mediated resistance to vascular pathogens. By combining transcriptomic and metabolomic data, we demonstrated a general repression of indole metabolism in wat1‐1 roots as shown by constitutive down‐regulation of several genes encoding proteins of the indole glucosinolate biosynthetic pathway and reduced amounts of tryptophan (Trp), indole‐3‐acetic acid and neoglucobrassicin, the major form of indole glucosinolate in roots. Furthermore, the susceptibility of the wat1 mutant to R. solanacearum was partially restored when crossed with either the trp5 mutant, an over‐accumulator of Trp, or Pro35S:AFB1‐myc, in which indole‐3‐acetic acid signaling is constitutively activated. Our original hypothesis placed cell‐wall modifications at the heart of the wat1 resistance phenotype. However, the results presented here suggest a mechanism involving root‐localized metabolic channeling away from indole metabolites to SA as a central feature of wat1 resistance to R. solanacearum.

Publications scientifiques (24) — classées par pathologie

Source PubMed · Recherche par auteur (homonymes possibles, vérifier l'affiliation).

Datasets & protocoles partagés

• Expression et régulation de l'antigène CD23 par les lymphocytes B de la leucémie lymphoïde chronique

  Dissertation1992Université de Montréal

  Thèse numérisée par la Direction des bibliothèques de l'Université de Montréal.

Source : DataCite — DOIs pour datasets, logiciels, protocoles, registres patient. Hors articles (déjà couverts).

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