Liste des publications scientifiques du CHU de Clermont-Ferrand

Cette liste prend en compte l'ensemble des publications scientifiques du CHU référencées sur PubMed de 1973 au 31.12.2020

Auteurs : Gross, C; Belville, C; Lavergne, M; Blanchon, L; Sapin, V ; et al.

Revue : Investigative ophthalmology & visual science - ISSN : 1552-5783 - NLMID : 7703701
Date de Publication : Mars 2020
Vol. : 61 Numéro 3 Pages : 14

Résumé : We used a human corneal epithelial cell (HCE) line to determine the involvement of the advanced glycation end products (AGEs) / receptor for AGEs (RAGE) couple in corneal epithelium wound healing.After wounding, HCE cells were exposed to two major RAGE ligands (HMGB1 and AGEs), and wound healing was evaluated using the in vitro scratch assay. Following wound healing, the HCE cells were used to study the influence of the RAGE ligands on HCE proliferation, invasion, and migration. Activation of the nuclear factor (NF)-?B signaling pathway by the AGEs/RAGE couple was tested using a luciferase reporter assay. Functional transcriptional regulation by this pathway was confirmed by quantification of expression of the connexin 43 target gene. For each experiment, specific RAGE involvement was confirmed by small interfering RNA treatments.AGEs treatment at a dose of 100 µg/mL significantly improved the wound healing process in a RAGE-dependent manner by promoting cell migration, whereas HMGB1 had no effect. No significant influence of the AGEs/RAGE couple was observed on cell proliferation and invasion. However, this treatment induced an early activation of the NF-?B pathway and positively regulated the expression of the target gene, connexin 43, at both the mRNA and protein levels.Our results demonstrate that the RAGE pathway is activated by AGEs treatment and is involved in the promotion of corneal epithelial wound healing. This positive action is observed only during the early stages of wound healing, as illustrated by the quick activation of the NF-?B pathway and induction of connexin 43 expression.

Mesh : Cell Line|Cell Movement/drug effects/physiology|Cell Proliferation/drug effects/physiology|Cells, Cultured|Connexin 43/genetics/metabolism|Corneal Injuries/pathology/physiopathology|Dose-Response Relationship, Drug|Epithelial Cells/drug effects/metabolism|Epithelium, Corneal/cytology/drug effects/injuries/physiology|Glycation End Products, Advanced/administration & dosage/pharmacology/physiology|HMGB1 Protein/administration & dosage/pharmacology|Humans|NF-kappa B/metabolism|RNA, Messenger/genetics|RNA, Small Interfering/genetics|Receptor for Advanced Glycation End Products/genetics/physiology|Signal Transduction/physiology|Wound Healing/drug effects/physiology

Auteurs : Dallel, R ;

Revue : Journal of neural transmission (Vienna, Austria : 1996) - ISSN : 1435-1463 - NLMID : 9702341
Date de Publication : Avril 2020
Vol. : 127 Numéro 4 Pages : 389-392
Auteurs : Touron, J; Costes, F; Coudeyre, E; Perrault, H; Richard, R ;

Revue : Frontiers in physiology - ISSN : 1664-042X - NLMID : 101549006
Date de Publication : Janvier 2020
Vol. : 11 Pages : 596351

Résumé : A characteristic feature of eccentric as compared with concentric exercise is the ability to generate greater mechanical loads for lower cardiopulmonary demands. Current evidence concurs to show that eccentric training translates into considerable gains in muscle mass and strength. Less is known, however, regarding its impact on oxygen transport and on factors to be considered for optimizing its prescription and monitoring. This article reviews the existing evidence for endurance eccentric exercise effects on the components of the oxygen transport system from systemic to mitochondria in both humans and animals. In the studies reviewed, specially designed cycle-ergometers or downhill treadmill running were used to generate eccentric contractions. Observations to date indicate that overall, the aerobic demand associated with the eccentric training load was too low to significantly increase peak maximal oxygen consumption. By extension, it can be inferred that the very high eccentric power output that would have been required to solicit a metabolic demand sufficient to enhance peak aerobic power could not be tolerated or sustained by participants. The impact of endurance eccentric training on peripheral flow distribution remains largely undocumented. Given the high damage susceptibility of eccentric exercise, the extent to which skeletal muscle oxygen utilization adaptations would be seen depends on the balance of adverse and positive signals on mitochondrial integrity. The article examines the protection provided by repeated bouts of acute eccentric exercise and reports on the impact of eccentric cycling and downhill running training programs on markers of mitochondrial function and of mitochondrial biogenesis using mostly from animal studies. The summary of findings does not reveal an impact of training on skeletal muscle mitochondrial respiration nor on selected mitochondrial messenger RNA transcripts. The implications of observations to date are discussed within future perspectives for advancing research on endurance eccentric exercise physiological impacts and using a combined eccentric and concentric exercise approach to optimize functional capacity.

Mots clés auteurs : /calcium/eccentric training/free radicals/mitochondria/oxygen consumption

Auteurs : Bouquier, N; Moutin, E; Tintignac, LA; Perroy, J; Ollendorff, V ; et al.

Revue : BMC biology - ISSN : 1741-7007 - NLMID : 101190720
Date de Publication : Juillet 2020
Vol. : 18 Numéro 1 Pages : 81

Résumé : mTOR signaling is an essential nutrient and energetic sensing pathway. Here we describe AIMTOR, a sensitive genetically encoded BRET (Bioluminescent Resonance Energy Transfer) biosensor to study mTOR activity in living cells.As a proof of principle, we show in both cell lines and primary cell cultures that AIMTOR BRET intensities are modified by mTOR activity changes induced by specific inhibitors and activators of mTORC1 including amino acids and insulin. We further engineered several versions of AIMTOR enabling subcellular-specific assessment of mTOR activities. We then used AIMTOR to decipher mTOR signaling in physio-pathological conditions. First, we show that mTORC1 activity increases during muscle cell differentiation and in response to leucine stimulation in different subcellular compartments such as the cytosol and at the surface of the lysosome, the nucleus, and near the mitochondria. Second, in hippocampal neurons, we found that the enhancement of neuronal activity increases mTOR signaling. AIMTOR further reveals mTOR-signaling dysfunctions in neurons from mouse models of autism spectrum disorder.Altogether, our results demonstrate that AIMTOR is a sensitive and specific tool to investigate mTOR-signaling dynamics in living cells and phenotype mTORopathies.

Mots clés auteurs : /Autism spectrum disorder/BRET/Muscle differentiation/Neuronal activity/mTORC1 Biosensor/mTor signaling/mToropathies

Auteurs : Wulf, GG; Altmann, B; Ziepert, M; Trümper, L; , ; et al.

Revue : Leukemia - ISSN : 1476-5551 - NLMID : 8704895
Date de Publication : Mai 2020

Résumé : PTCL patients exhibit poor survival with existing treatments. We investigated the efficacy of CHOP combined with alemtuzumab in 116 PTCL patients age 61-80 in an open-label, randomized phase 3 trial. Alemtuzumab was given on day 1, to a total of 360?mg in 21 patients, or 120?mg in 37. Hematotoxicity was increased with A-CHOP resulting in more grade ?3 infections (40% versus 21%) and 4 versus 1 death due to infections, respectively. CR/CRu rate was 60% for A-CHOP and 43% for CHOP, and OR rate was 72% and 66%, respectively. Three-year-EFS, PFS and OS were 27% [15%-39%], 28% [15%-40%], and 37% ([23%-50%] for A-CHOP, and 24% [12%-35%], 29% [17%-41%], and 56% [44%-69%] for CHOP, respectively, showing no significant differences. Multivariate analyses, adjusted for strata and sex confirmed these results (hazard ratio HREFS: 0.7 ([95% CI: 0.5-1.1]; p?=?0.094), HRPFS: 0.8 ([95% CI: 0.5-1.2]; p?=?0.271), HROS: 1.4 ([95% CI: 0.9-2.4]; p?=?0.154). The IPI score was validated, and male sex (HREFS 2.5) and bulky disease (HREFS 2.2) were significant risk factors for EFS, PFS, and OS. Alemtuzumab added to CHOP increased response rates, but did not improve survival due to treatment-related toxicity.