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5. Mechanisms involved in cardioprotective effects of pravastatin administered during reoxygenation in human myocardium in vitro

Author

Lemoine, S, Allouche, S, Coulbault, L, Cornet, V, Massetti, Massimo, Galera, P, Gérard, J, Hanouz, J., Massetti, Massimo (ORCID:0000-0002-7100-8478), Lemoine, S, Allouche, S, Coulbault, L, Cornet, V, Massetti, Massimo, Galera, P, Gérard, J, Hanouz, J., and Massetti, Massimo (ORCID:0000-0002-7100-8478)

Abstract

The authors investigated the effect of pravastatin during reoxygenation after myocardial hypoxia and examined the involvement of nitric oxide synthase, mitochondrial permeability transition pore, and expression of markers of apoptosis in human myocardium in vitro.

Published
2012

6. Poster session 3

Author

Nanka, O., primary, Krejci, E., additional, Pesevski, Z., additional, Sedmera, D., additional, Smart, N., additional, Rossdeutsch, A., additional, Dube, K. N., additional, Riegler, J., additional, Price, A. N., additional, Taylor, A., additional, Muthurangu, V., additional, Turner, M., additional, Lythgoe, M. F., additional, Riley, P. R., additional, Kryvorot, S., additional, Vladimirskaya, T., additional, Shved, I., additional, Schwarzl, M., additional, Seiler, S., additional, Huber, S., additional, Steendijk, P., additional, Maechler, H., additional, Truschnig-Wilders, M., additional, Pieske, B., additional, Post, H., additional, Caprio, C., additional, Baldini, A., additional, Chiavacci, E., additional, Dolfi, L., additional, Verduci, L., additional, Meghini, F., additional, Cremisi, F., additional, Pitto, L., additional, Kuan, T.-C., additional, Chen, M.-C., additional, Yang, T.-H., additional, Wu, W.-T., additional, Lin, C. S., additional, Rai, H., additional, Kumar, S., additional, Sharma, A. K., additional, Mastana, S., additional, Kapoor, A., additional, Pandey, C. M., additional, Agrawal, S., additional, Sinha, N., additional, Orlowska-Baranowska, E. H., additional, Placha, G., additional, Gora, J., additional, Baranowski, R., additional, Abramczuk, E., additional, Hryniewiecki, T., additional, Gaciong, Z., additional, Verschuren, J. J. W., additional, Wessels, J. A. M., additional, Trompet, S., additional, Stott, D. J., additional, Sattar, N., additional, Buckley, B., additional, Guchelaar, H. J., additional, Jukema, J. W., additional, Gharanei, M., additional, Hussain, A., additional, Mee, C. J., additional, Maddock, H. L., additional, Wijnen, W. J., additional, Van Den Oever, S., additional, Van Der Made, I., additional, Hiller, M., additional, Tijsen, A. J., additional, Pinto, Y. M., additional, Creemers, E. E., additional, Nikulina, S. U. Y., additional, Chernova, A., additional, Petry, A., additional, Rzymski, T., additional, Kracun, D., additional, Riess, F., additional, Pike, L., additional, Harris, A. L., additional, Gorlach, A., additional, Katare, R., additional, Oikawa, A., additional, Riu, F., additional, Beltrami, A. P., additional, Cesseli, D., additional, Emanueli, C., additional, Madeddu, P., additional, Zaglia, T., additional, Milan, G., additional, Franzoso, M., additional, Pesce, P., additional, Sarais, C., additional, Sandri, M., additional, Mongillo, M., additional, Butler, T. J., additional, Seymour, A.-M. L., additional, Ashford, D., additional, Jaffre, F., additional, Bussen, M., additional, Flohrschutz, I., additional, Martin, G. R., additional, Engelhardt, S., additional, Kararigas, G., additional, Nguyen, B. T., additional, Jarry, H., additional, Regitz-Zagrosek, V., additional, Van Bilsen, M., additional, Daniels, A., additional, Munts, C., additional, Janssen, B. J. A., additional, Van Der Vusse, G. J., additional, Van Nieuwenhoven, F. A., additional, Montalvo, C., additional, Villar, A. V., additional, Merino, D., additional, Garcia, R., additional, Llano, M., additional, Ares, M., additional, Hurle, M. A., additional, Nistal, J. F., additional, Dembinska-Kiec, A., additional, Beata Kiec-Wilk, B. K. W., additional, Anna Polus, A. P., additional, Urszula Czech, U. C., additional, Tatiana Konovaleva, T. K., additional, Gerd Schmitz, G. S., additional, Bertrand, L., additional, Balteau, M., additional, Timmermans, A., additional, Viollet, B., additional, Sakamoto, K., additional, Feron, O., additional, Horman, S., additional, Vanoverschelde, J. L., additional, Beauloye, C., additional, De Meester, C., additional, Martinez, E., additional, Martin, R., additional, Miana, M., additional, Jurado, R., additional, Gomez-Hurtado, N., additional, Bartolome, M. V., additional, San Roman, J. A., additional, Lahera, V., additional, Nieto, M. L., additional, Cachofeiro, V., additional, Rochais, F., additional, Sturny, R., additional, Mesbah, K., additional, Miquerol, L., additional, Kelly, R. G., additional, Messaoudi, S., additional, Gravez, B., additional, Tarjus, A., additional, Pelloux, V., additional, Samuel, J. L., additional, Delcayre, C., additional, Launay, J. M., additional, Clement, K., additional, Farman, N., additional, Jaisser, F., additional, Hadyanto, L., additional, Castellani, C., additional, Vescovo, G., additional, Ravara, B., additional, Tavano, R., additional, Pozzobon, M., additional, De Coppi, P., additional, Papini, E., additional, Vettor, R., additional, Thiene, G., additional, Angelini, A., additional, Meloni, M., additional, Caporali, A., additional, Cesselli, D., additional, Fortunato, O., additional, Avolio, E., additional, Schindler, R., additional, Simrick, S., additional, Brand, T., additional, Smart, N. 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Published
2012
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8. In vitro and in vivo pharmacological profile of UFP-512, a novel selective delta-opioid receptor agonist; correlations between desensitization and tolerance.

Author

Aguila, B., Coulbault, L., Boulouard, M., Lıveillı, F., Davis, A., Tσth, G., Borsodi, A., Balboni, G., Salvadori, S., Jauzac, P., Allouche, S., Léveillé, F, and Tóth, G

Subjects
*PHARMACOLOGY, *MEDICAL sciences, *OPIOID receptors, *DESENSITIZATION (Psychotherapy), *MENTAL depression, *ANTIDEPRESSANTS, *TRANQUILIZING drugs, *NEUROBLASTOMA, *ALLERGY desensitization, *BIOLOGICAL models, *BINDING sites, *RESEARCH, *DRUG tolerance, *MITOXANTRONE, *HETEROCYCLIC compounds, *OLIGOPEPTIDES, *ANIMAL experimentation, *RESEARCH methodology, *CELL receptors, *ANTINEOPLASTIC agents, *MEDICAL cooperation, *EVALUATION research, *DRUG administration, *CELLULAR signal transduction, *COMPARATIVE studies, *TRANSFERASES, *CYTARABINE, *SWIMMING, *ENDOCYTOSIS, *PREDNISONE, *CELL lines, *PHOSPHORYLATION, *MICE, *PHARMACODYNAMICS
Abstract

Background and Purpose: Delta-opioid receptors (DOP receptors) could represent a novel target in the treatment of depressive disorders. To explore this new field of interest, the development of highly selective DOP receptor agonists is essential. UFP-512 [H-Dmt-Tic-NH-CH(CH2-COOH)-Bid], was recently shown to behave in vitro as a selective and potent DOP receptor agonist and to promote antidepressant- and anxiolytic-like effects in vivo (Vergura et al., 2007). Here, we have characterized the pharmacological properties of UFP-512 and established a link between desensitization and tolerance.Experimental Approach: Studies were performed in the human neuroblastoma SK-N-BE cells to establish i) binding parameters for UFP-512 ii) signalling pathways activated after acute and chronic treatment iii) regulation (phosphorylation and trafficking) of human DOP (hDOP) receptors after sustained activation by UFP-512. In vivo, we studied UFP-512-induced antidepressant-like effects after acute or chronic treatment in the mouse forced swimming test.Key Results: In vitro, UFP-512 was a high affinity agonist for DOP receptors. While UFP-512 induced marked phosphorylation of DOP receptors on Ser363, we observed a low desensitization of the cAMP pathway, associated with receptor endocytosis and recycling without any reduction on extracellular signal-regulated protein kinase 1/2 activation. In vivo, acute administration of UFP-512 produced an antidepressant-like effect, without any sign of tolerance after chronic administration.Conclusions and Implications: There was a correlation between weak desensitization, significant internalization and recycling of the human DOP receptors and lack of tolerance to UFP-512. This suggests that this compound would be a promising drug prototype for exploring innovative treatments for mood disorders. [ABSTRACT FROM AUTHOR]

Published
2007
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11. Alcohol Withdrawal Is an Oxidative Stress Challenge for the Brain: Does It Pave the Way toward Severe Alcohol-Related Cognitive Impairment?

Author

Clergue-Duval V, Coulbault L, Questel F, Cabé N, Laniepce A, Delage C, Boudehent C, Bloch V, Segobin S, Naassila M, Pitel AL, and Vorspan F

Abstract

Alcohol use is a leading cause of mortality, brain morbidity, neurological complications and minor to major neurocognitive disorders. Alcohol-related neurocognitive disorders are consecutive to the direct effect of chronic and excessive alcohol use, but not only. Indeed, patients with severe alcohol use disorders (AUD) associated with pharmacological dependence suffer from repetitive events of alcohol withdrawal (AW). If those AW are not managed by adequate medical and pharmacological treatment, they may evolve into severe AW, or be complicated by epileptic seizure or delirium tremens (DT). In addition, we suggest that AW favors the occurrence of Wernicke's encephalopathy (WE) in patients with known or unknown thiamine depletion. We reviewed the literature on oxidative stress as a core mechanism in brain suffering linked with those conditions: AW, epileptic seizure, DT and WE. Thus, we propose perspectives to further develop research projects aiming at better identifying oxidative stress brain damage related to AW, assessing the effect of repetitive episodes of AW, and their long-term cognitive consequences. This research field should develop neuroprotective strategies during AW itself or during the periwithdrawal period. This could contribute to the prevention of severe alcohol-related brain damage and cognitive impairments.

Published
2022
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12. Trimethylamine N -Oxide (TMAO) and Indoxyl Sulfate Concentrations in Patients with Alcohol Use Disorder.

Author

Coulbault L, Laniepce A, Segobin S, Boudehent C, Cabé N, and Pitel AL

Subjects
Biomarkers, Humans, Indican, Methylamines, Prealbumin, Alcoholism, Substance Withdrawal Syndrome
Abstract

Background: Trimethylamine N -oxide (TMAO) and indoxyl sulfate (IS) are produced by the microbiota and the liver, and can contribute to brain aging and impaired cognitive function. This study aims to examine serum TMAO and IS concentrations in patients with alcohol-use disorder (AUD) at the entry for alcohol withdrawal, and the relationships with several biological, neuropsychological, and clinical parameters., Methods: TMAO and IS were quantified in thirty AUD inpatients and fifteen healthy controls (HC). The severities of AUD and alcohol withdrawal syndrome (AWS), and general cognitive abilities were assessed in AUD patients., Results: TMAO concentrations did not differ between HC and AUD patients. Several biomarkers assessing nutritional status and liver function were significantly different in AUD patients with the lowest TMAO concentrations compared to other AUD patients. IS concentration was significantly lower in AUD patients and a significant positive predictor of serum prealbumin variation during the acute phase of alcohol withdrawal. No relationship was observed between the concentrations of these metabolites and the severities of alcohol dependence, AWS, or cognitive deficits., Conclusions: Our data suggest that AUD patients with low concentrations of TMAO or IS should probably benefit from a personalized refeeding program during the acute phase of alcohol withdrawal.

Published
2022
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13. Role of inflammation in alcohol-related brain abnormalities: a translational study.

Author

Lanquetin A, Leclercq S, de Timary P, Segobin S, Naveau M, Coulbault L, Maccioni P, Lorrai I, Colombo G, Vivien D, Rubio M, and Pitel AL

Abstract

Brain abnormalities observed in alcohol use disorder are highly heterogeneous in nature and severity, possibly because chronic alcohol consumption also affects peripheral organs leading to comorbidities that can result in exacerbated brain alterations. Despite numerous studies focussing on the effects of alcohol on the brain or liver, few studies have simultaneously examined liver function and brain damage in alcohol use disorder, and even fewer investigated the relationship between them except in hepatic encephalopathy. And yet, liver dysfunction may be a risk factor for the development of alcohol-related neuropsychological deficits and brain damage well before the development of liver cirrhosis, and potentially through inflammatory responses. The use of animal models enables a better understanding of the pathophysiological mechanisms underlying liver-brain relationships in alcohol use disorder, and more particularly of the inflammatory response at the tissue, cerebral and hepatic levels. The objective of this translational study was to investigate, both in alcohol use disorder patients and in a validated animal model of alcohol use disorder, the links between peripheral inflammation, liver damage and brain alterations. To do this, we conducted an in vivo neuroimaging examination and biological measures to evaluate brain volumes, liver fibrosis and peripheral cytokines in alcohol use disorder patients. In selectively bred Sardinian alcohol-preferring rats, we carried out ex vivo neuroimaging examination and immunohistochemistry to evaluate brain and liver inflammatory responses after chronic (50 consecutive weeks) alcohol drinking. In recently abstinent and non-cirrhotic alcohol use disorder patients, the score of liver fibrosis positively correlated with subcortical regions volumes (especially in right and left putamen) and level of circulating proinflammatory cytokines. In Sardinian alcohol-preferring rats, we found macrostructural brain damage and microstructural white matter abnormalities similar to those found in alcohol use disorder patients. In addition, in agreement with the results of peripheral inflammation observed in the patients, we revealed, in Sardinian alcohol-preferring rats, inflammatory responses in the brain and liver were caused by chronic alcohol consumption. Since the liver is the main source of cytokines in the human body, these results suggest a relationship between liver dysfunction and brain damage in alcohol use disorder patients, even in the absence of major liver disease. These findings encourage considering new therapeutic strategies aiming at treating peripheral organs to limit alcohol-related brain damage., (© The Author(s) (2021). Published by Oxford University Press on behalf of the Guarantors of Brain.)

Published
2021
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14. Nicotinamide Deficiency in Primary Open-Angle Glaucoma.

Author

Kouassi Nzoughet J, Chao de la Barca JM, Guehlouz K, Leruez S, Coulbault L, Allouche S, Bocca C, Muller J, Amati-Bonneau P, Gohier P, Bonneau D, Simard G, Milea D, Lenaers G, Procaccio V, and Reynier P

Subjects
Adult, Aged, Aged, 80 and over, Case-Control Studies, Chromatography, Liquid, Cohort Studies, Female, Glaucoma, Open-Angle diagnosis, Humans, Intraocular Pressure, Male, Middle Aged, Spectrometry, Mass, Electrospray Ionization, Glaucoma, Open-Angle blood, Niacinamide deficiency
Abstract

Purpose: To investigate the plasma concentration of nicotinamide in primary open-angle glaucoma (POAG)., Methods: Plasma of 34 POAG individuals was compared to that of 30 age- and sex-matched controls using a semiquantitative method based on liquid chromatography coupled to high-resolution mass spectrometry. Subsequently, an independent quantitative method, based on liquid chromatography coupled to mass spectrometry, was used to assess nicotinamide concentration in the plasma from the same initial cohort and from a replicative cohort of 20 POAG individuals and 15 controls., Results: Using the semiquantitative method, the plasma nicotinamide concentration was significantly lower in the initial cohort of POAG individuals compared to controls and further confirmed in the same cohort, using the targeted quantitative method, with mean concentrations of 0.14 μM (median: 0.12 μM; range, 0.06-0.28 μM) in the POAG group (-30%; P = 0.022) and 0.19 μM (median: 0.18 μM; range, 0.08-0.47 μM) in the control group. The quantitative dosage also disclosed a significantly lower plasma nicotinamide concentration (-33%; P = 0.011) in the replicative cohort with mean concentrations of 0.14 μM (median: 0.14 μM; range, 0.09-0.25 μM) in the POAG group, and 0.19 μM (median: 0.21 μM; range, 0.09-0.26 μM) in the control group., Conclusions: Glaucoma is associated with lower plasmatic nicotinamide levels, compared to controls, suggesting that nicotinamide supplementation might become a future therapeutic strategy. Further studies are needed, in larger cohorts, to confirm these preliminary findings.

Published
2019
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15. Clinical and Biological Risk Factors for Neuropsychological Impairment in Alcohol Use Disorder.

Author

Ritz L, Coulbault L, Lannuzel C, Boudehent C, Segobin S, Eustache F, Vabret F, Pitel AL, and Beaunieux H

Subjects
Adult, Case-Control Studies, Female, Humans, Male, Middle Aged, Risk Factors, Alcoholism psychology, Neuropsychological Tests
Abstract

The effects of alcoholism on cognitive and motor functioning are heterogeneous. While the role of some factors (patterns of alcohol consumption, eating habits or associated liver disease) has been hypothesized, the origins of this heterogeneity remain difficult to establish. The goals of the present study were thus to identify the clinical and biological risk factors for alcohol-related neuropsychological impairments and to determine the threshold beyond which these risk factors can be considered significant. Thirty alcoholic patients and 15 healthy controls had a blood test and underwent a neuropsychological examination. Alcohol severity measures, and liver, thiamine and malnutrition variables, were included in logistic regression models to determine the risk factors for cognitive and motor impairments (executive functions, visuospatial abilities, verbal episodic memory, ataxia), as well as those related to the severity of patients' overall neuropsychological profile (moderate or severe impairments). Liver fibrosis was found to be a risk factor for executive impairments and also for ataxia, when it was associated with long-term alcohol misuse and symptoms of withdrawal. Altered thiamine metabolism was solely predictive of verbal episodic memory impairments. This combination of biological abnormalities was associated with a profile of moderate neuropsychological impairments. Malnutrition was associated with a profile of more severe impairments. Malnutrition, altered liver function and thiamine metabolism explain, at least partially, the heterogeneity of alcohol-related neuropsychological impairments. Our findings could allow clinicians to identify patients at particular risk of severe neuropsychological impairments before the onset of irreversible and debilitating neurological complications., Competing Interests: The authors have declared that no competing interests exist.

Published
2016
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16. Hyperglycemia-Induced Hypovolemia Is Involved in Early Cardiac Magnetic Resonance Alterations in Streptozotocin-Induced Diabetic Mice: A Comparison with Furosemide-Induced Hypovolemia.

Author

Joubert M, Bellevre D, Legallois D, Elie N, Coulbault L, Allouche S, and Manrique A

Subjects
Animals, Diabetes Mellitus, Experimental pathology, Hyperglycemia pathology, Hypovolemia pathology, Male, Mice, Cardiac Imaging Techniques, Diabetes Mellitus, Experimental physiopathology, Furosemide, Hyperglycemia complications, Hyperglycemia physiopathology, Hypovolemia chemically induced, Hypovolemia complications, Magnetic Resonance Imaging
Abstract

Aims: The aim of the study was to assess the early features of diabetic cardiomyopathy using cardiac magnetic resonance within the first week after streptozotocin injection in mice. We focused on the relationship between left ventricular function and hypovolemia markers in diabetic animals compared to a hypovolemic rodent model., Methods and Results: Swiss mice were randomized into control (group C), streptozotocin-induced diabetes (group D) and furosemide-induced hypovolemia (group F) groups. Cardiac magnetic resonance, non-invasive blood pressure, urine volume, plasma markers of dehydration and cardiac histology were assessed in all groups. Mean blood glucose was higher in diabetic animals than in groups C and F (30.5±5.8 compared to 10.4±2.1 and 11.1±2.8 mmol/L, respectively; p<0.01). Diuresis was increased in animals from group D and F compared to C (14650±11499 and 1533±540 compared to 192±111 μL/24 h; p<0.05). End diastolic and end systolic volumes were lower in group D than in group C at week 1 (1.52±0.36 vs. 1.93±0.35 and 0.54±0.22 vs. 0.75±0.18 mL/kg, p<0.05). These left ventricular volume values in group D were comparable to those observed in the acute hypovolemia model (group F). Increased dehydration plasma markers and an absence of obvious intrinsic myocardial damage (evaluated by cardiac magnetic resonance and histology) suggest that a hemodynamic mechanism underlies the very early drop in left ventricular volumes in group D and provides a potential link to hyperglycemic osmotic diuresis., Conclusions: Researchers using cardiac magnetic resonance in hyperglycemic rodent models should be aware of this hemodynamic mechanism, which may partially explain modifications in cardiac parameters in addition to diabetic myocardial damage.

Published
2016
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17. TRPM4 non-selective cation channels influence action potentials in rabbit Purkinje fibres.

Author

Hof T, Sallé L, Coulbault L, Richer R, Alexandre J, Rouet R, Manrique A, and Guinamard R

Subjects
Animals, Calcium metabolism, Cells, Cultured, Female, Myocytes, Cardiac physiology, Potassium metabolism, Purkinje Fibers cytology, Purkinje Fibers physiology, Rabbits, Sodium metabolism, Action Potentials, Myocytes, Cardiac metabolism, Purkinje Fibers metabolism, TRPM Cation Channels metabolism
Abstract

Key Points: The transient receptor potential melastatin 4 (TRPM4) inhibitor 9-phenanthrol reduces action potential duration in rabbit Purkinje fibres but not in ventricle. TRPM4-like single channel activity is observed in isolated rabbit Purkinje cells but not in ventricular cells. The TRPM4-like current develops during the notch and early repolarization phases of the action potential in Purkinje cells., Abstract: Transient receptor potential melastatin 4 (TRPM4) Ca(2+)-activated non-selective cation channel activity has been recorded in cardiomyocytes and sinus node cells from mammals. In addition, TRPM4 gene mutations are associated with human diseases of cardiac conduction, suggesting that TRPM4 plays a role in this aspect of cardiac function. Here we evaluate the TRPM4 contribution to cardiac electrophysiology of Purkinje fibres. Ventricular strips with Purkinje fibres were isolated from rabbit hearts. Intracellular microelectrodes recorded Purkinje fibre activity and the TRPM4 inhibitor 9-phenanthrol was applied to unmask potential TRPM4 contributions to the action potential. 9-Phenanthrol reduced action potential duration measured at the point of 50 and 90% repolarization with an EC50 of 32.8 and 36.1×10(-6) mol l(-1), respectively, but did not modulate ventricular action potentials. Inside-out patch-clamp recordings were used to monitor TRPM4 activity in isolated Purkinje cells. TRPM4-like single channel activity (conductance = 23.8 pS; equal permeability for Na(+) and K(+); sensitivity to voltage, Ca(2+) and 9-phenanthrol) was observed in 43% of patches from Purkinje cells but not from ventricular cells (0/16). Action potential clamp experiments performed in the whole-cell configuration revealed a transient inward 9-phenanthrol-sensitive current (peak density = -0.65 ± 0.15 pA pF(-1); n = 5) during the plateau phases of the Purkinje fibre action potential. These results show that TRPM4 influences action potential characteristics in rabbit Purkinje fibres and thus could modulate cardiac conduction and be involved in triggering arrhythmias., (© 2015 The Authors. The Journal of Physiology © 2015 The Physiological Society.)

Published
2016
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