A5002023781- Pancreatic function and diabetes
- Liver Disease Diagnosis and Treatment
- Metabolism, Diabetes, and Cancer
- Hepatitis C virus research
- Immunotherapy and Immune Responses
- Cell death mechanisms and regulation
- Melanoma and MAPK Pathways
- Endoplasmic Reticulum Stress and Disease
- Diabetes and associated disorders
- CAR-T cell therapy research
- Gut microbiota and health
- Inflammatory Bowel Disease
- Neuroscience and Neuropharmacology Research
- Hepatitis B Virus Studies
- RNA Interference and Gene Delivery
- Diet, Metabolism, and Disease
- Protein Kinase Regulation and GTPase Signaling
- Cancer Research and Treatments
- Hearing, Cochlea, Tinnitus, Genetics
- Liver Disease and Transplantation
- Cardiac Ischemia and Reperfusion
- Clostridium difficile and Clostridium perfringens research
- FOXO transcription factor regulation
- Cancer Immunotherapy and Biomarkers
- Anesthesia and Sedative Agents
Enterome (France)
2017-2025
Lifetech Scientific (China)
2024
ReShape Lifesciences (United States)
2017
Centre Hospitalier Universitaire de Clermont-Ferrand
2004-2015
Clinique Ambroise Paré
2011-2015
University of Lausanne
1995-2014
University Hospital of Lausanne
2003-2014
Xigen (Switzerland)
2007-2013
Université Clermont Auvergne
2011
Hôtel-Dieu de Lyon
2005-2010
Stress conditions and proinflammatory cytokines activate the c-Jun NH2-terminal kinase (JNK), a member of stress-activated group mitogen-activated protein kinases (MAPKs). We recently demonstrated that inhibition JNK signaling with use islet-brain (IB) 1 2 proteins prevented interleukin (IL)-1beta-induced pancreatic beta-cell death. Bioactive cell-permeable peptide inhibitors were engineered by linking minimal 20-amino acid inhibitory domains IB to 10-amino HIV-TAT sequence rapidly...
Optimal management of neuropathic pain is a major clinical challenge. We investigated the involvement c-Jun N-terminal kinase (JNK) in produced by spinal nerve ligation (SNL) (L5). SNL induced slow (>3 d) and persistent (>21 activation JNK, particular JNK1, GFAP-expressing astrocytes cord. In contrast, p38 mitogen-activated protein was found microglia after SNL, which had fallen to near basal level 21 d. Intrathecal infusion JNK peptide inhibitor, D-JNKI-1, did not affect normal responses...
Hearing loss can be caused by a variety of insults, including acoustic trauma and exposure to ototoxins, that principally effect the viability sensory hair cells via MAP kinase (MAPK) cell death signaling pathway incorporates c-Jun N-terminal (JNK). We evaluated otoprotective efficacy D-JNKI-1, permeable peptide blocks MAPK-JNK signal pathway. The experimental studies included organ cultures neonatal mouse cochlea exposed an ototoxic drug cochleae adult guinea pigs were either or trauma....
The homeodomain protein PDX-1, referred as IPF-1/STF-1/IDX-1, is a transcriptional factor that plays critical role in the control of several genes expressed pancreatic islet. PDX-1 gene expression has been previously shown to be reduced cultured beta-cell lines chronically exposed high glucose concentrations. As transporter type 2 (GLUT2) selectively decreased beta-pancreatic cells experimental models diabetes, we postulated loss GLUT2 islets diabetic animals may due transacting function on...
IDX-1 (islet/duodenum homeobox-1) is a transcription factor expressed in the duodenum and pancreatic beta delta cells. It required for embryonic development of pancreas transactivates theGlut2, glucokinase, insulin, somatostatin genes. Here we show that exposure isolated rat islets to palmitic acid induced ∼70% decrease mRNA protein expression as well 40 65% decreases binding activity its cognate cis-regulatory elements theGlut2 insulin promoters, respectively. The inhibitory effect...
To characterize the differentiation events that selectively target insulin-producing cells to interleukin (IL)-1beta-induced apoptosis, we studied IL-1beta signaling via mitogen-activated protein kinase (MAPK) and stress-activated in 2 pancreatic endocrine cell lines. We glucagon-secreting AN-glu line insulin islet amyloid polypeptide-producing beta-cell (AN-ins cells), which is derived by stable transfection of with transcription factor duodenal homeobox factor-1. AN-ins were more sensitive...
Macrophage migration inhibitory factor (MIF), originally identified as a cytokine secreted by T lymphocytes, was found recently to be both pituitary hormone and mediator released immune cells in response glucocorticoid stimulation. We report here that the insulin-secreting β cell of islets Langerhans expresses MIF its production is regulated glucose time- concentration-dependent manner. insulin colocalize immunocytochemistry within secretory granules pancreatic islet cells, once released,...
Pancreatic islet transplantation may successfully restore normoglycemia in type 1 diabetic patients. However, successful grafting requires of a sufficient number islets, usually requiring two or more donors. During the isolation process and following clinical transplantation, islets are subjected to severe adverse conditions that impair survival ultimately contribute graft failure. Here, we have mapped major intracellular stress-signaling pathways mediate human loss during cytokine attack....
JIP-1 is a cytoplasmic inhibitor of the c-Jun amino-terminal kinase activated pathway recently cloned from mouse brain cDNA library. We report herein expression cloning rat encoding JIP-1-related nuclear protein pancreatic beta-cell library that we named IB1 for Islet-Brain 1. was isolated by its ability to bind GTII, cis-regulatory element GLUT2 promoter. The encodes 714-amino acid protein, which differs insertion 47 amino acids in carboxyl-terminal part protein. remaining 667 are 97%...
We tested and characterized the therapeutic value of round window membrane-delivered (RWM) d-JNKI-1 peptide (Bonny et al., 2001) against sound trauma-induced hearing loss. Morphological characteristics sound-damaged hair cell nuclei labeled by Hoechst staining show that apoptosis is predominant mode death after trauma. Analysis events occurring trauma demonstrates c-Jun N-terminal kinase (JNK)/stress-activated protein activates a mitochondrial pathway (i.e., activation Bax, release...
In 2 models of severe ischemic injury, we have evaluated the neuroprotective action D-JNKI1, a cell-penetrating and protease-resistant peptide selectively inhibiting c-Jun-N-terminal kinase (JNK).Hippocampal slices from newborn rats were subjected to oxygen (5%) glucose (1 mmol/L) deprivation for 30 minutes. Cell death was with propidium iodide, evoked potential responses recorded in CA1 region after stimulation CA3. Male ICR-CD1 mice permanent endoluminal "suture" middle cerebral artery...
c-Jun N-terminal kinases (SAPK/JNKs) are activated by inflammatory cytokines, and JNK signaling is involved in insulin resistance beta-cell secretory function survival.Chronic high glucose concentrations leptin induce interleukin-1beta (IL-1beta) secretion from pancreatic islets, an event that possibly causal promoting dysfunction death.The present study provides evidence chronically elevated of apoptosis through activation the pathway human islets insulinoma (INS 832/13) cells.JNK...
Neuronal nitric oxide synthase (nNOS) and p38MAPK are strongly implicated in excitotoxicity, a mechanism common to many neurodegenerative conditions, but the intermediary is unclear. NOS1AP encoded by gene recently associated with sudden cardiac death, diabetes-associated complications, schizophrenia (Arking et al., 2006; Becker 2008; Brzustowicz, Lehtinen 2008). Here we find it interacts p38MAPK-activating kinase MKK3. Excitotoxic stimulus induces recruitment of nNOS rat cortical neuron...
BackgroundBariatric surgery is an effective therapeutic procedure for morbidly obese patients. The 2 most common interventions are sleeve gastrectomy (SG) and laparoscopic Roux-en-Y gastric bypass (LRYGB).ObjectivesThe aim of this study was to compare microbiome long-term after SG LRYGB in patients.SettingUniversity Hospital, France; University United States; Switzerland.MethodsEighty-nine 108 patients who underwent LRYGB, respectively, were recruited. Stools collected before 6 months...
IB1/JIP-1 is a scaffold protein that interacts with upstream components of the c-Jun N-terminal kinase (JNK) signaling pathway. IB1 expressed at high levels in pancreatic beta cells and may therefore exert tight control on events mediated by JNK these cells. Activation interleukin 1 (IL-1beta) or constitutive activator DeltaMEKK1 promoted apoptosis two cell lines decreased content 50-60%. To study functional consequences reduced lines, we used an insulin-secreting line expressing inducible...
Abstract: Background: The question of which colloid (albumin or synthetic colloids) used for plasma expansion following paracentesis other complications requiring fluid loading in patients with cirrhosis remains controversial. Aims: To compare outcome and hospital‐related cost treated 20% human albumin those a (3.5% polygeline). Methods: primary end point was occurrence first liver‐related complication. Results: When the trial prematurely discontinued because safety concerns about...
The c-Jun NH(2)-terminal kinase (JNK) pathway of the mitogen-activated protein (MAPK) signaling cascade regulates cell function and survival after stress stimulation. Equally robust studies reported dichotomous results suggesting both protective detrimental effects JNK during myocardial ischemia-reperfusion (I/R). lack a highly specific inhibitor contributed to this controversy. We recently developed cell-penetrating, protease-resistant peptide JNK, d-JNKI-1. Here we report on d-JNKI-1 in...
Abstract Background An Escherichia coli ( E. ) pathotype with invasive properties, first reported by Darfeuille-Michaud and termed adherent-invasive (AIEC), was shown to be prevalent in up half the individuals Crohn’s Disease (CD), suggesting that these bacteria could involved pathophysiology of CD. Among genes related AIEC pathogenicity, fim has potential generate an inflammatory reaction from intestinal epithelial cells macrophages, as it interacts TLR4, inducing production cytokines...