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Your search keyword '"Pradere, Jean-Philippe"' showing total 26 results
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26 results on '"Pradere, Jean-Philippe"'

1. Extracellular vesicles are carriers of adiponectin with insulin-sensitizing and anti-inflammatory properties

Author

Blandin, Alexia, Amosse, Jérémy, Froger, Josy, Hilairet, Grégory, Durcin, Maëva, Fizanne, Lionel, Ghesquière, Valentine, Prieur, Xavier, Chaigneau, Julien, Vergori, Luisa, Dray, Cédric, Pradère, Jean-Philippe, Blandin, Stéphanie, Dupont, Joëlle, Ducluzeau, Pierre-Henri, Dubois, Séverine, Boursier, Jérôme, Cariou, Bertrand, and Le Lay, Soazig

Published
2023
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3. HMGB1 links chronic liver injury to progenitor responses and hepatocarcinogenesis

Author

Hernandez, Celine, Huebener, Peter, Pradere, Jean-Philippe, Antoine, Daniel J., Friedman, Richard A., and Schwabe, Robert F.

Subjects
Liver diseases -- Genetic aspects -- Development and progression -- Research, Carcinogenesis -- Research, Promoters (Genetics) -- Research, Health care industry
Abstract

Cell death is a key driver of disease progression and carcinogenesis in chronic liver disease (CLD), highlighted by the well-established clinical correlation between hepatocellular death and risk for the development of cirrhosis and hepatocellular carcinoma (HCC). Moreover, hepatocellular death is sufficient to trigger fibrosis and HCC in mice. However, the pathways through which cell death drives CLD progression remain elusive. Here, we tested the hypothesis that high-mobility group box 1 (HMGB1), a damage-associated molecular pattern (DAMP) with key roles in acute liver injury, may link cell death to injury responses and hepatocarcinogenesis in CLD. While liver-specific HMGB1 deficiency did not significantly affect chronic injury responses such as fibrosis, regeneration, and inflammation, it inhibited ductular/progenitor cell expansion and hepatocyte metaplasia. HMGB1 promoted ductular expansion independently of active secretion in a nonautonomous fashion, consistent with its role as a DAMP. Liver-specific HMGB1 deficiency reduced HCC development in 3 mouse models of chronic injury but not in a model lacking chronic liver injury. As with CLD, HMGB1 ablation reduced the expression of progenitor and oncofetal markers, a key determinant of HCC aggressiveness, in tumors. In summary, HMGB1 links hepatocyte death to ductular reaction, progenitor signature, and hepatocarcinogenesis in CLD., Introduction Chronic liver disease (CLD) causes approximately 2 million deaths per year worldwide (1). In patients with CLD, liver cirrhosis and hepatocellular carcinoma (HCC) are the main contributors to morbidity [...]

Published
2018
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4. The HMGB1/RAGE axis triggers neutrophil-mediated injury amplification following necrosis

Author

Huebener, Peter, Pradere, Jean-Philippe, Hernandez, Celine, Gwak, Geum-Youn, Caviglia, Jorge Matias, Mu, Xueru, Loike, John D., Jenkins, Rosalind E., Antoine, Daniel J., and Schwabe, Robert F.

Subjects
Cell death -- Physiological aspects, Inflammation -- Physiological aspects -- Causes of, Necrosis -- Physiological aspects -- Genetic aspects, Health care industry
Abstract

In contrast to microbially triggered inflammation, mechanisms promoting sterile inflammation remain poorly understood. Damage-associated molecular patterns (DAMPs) are considered key inducers of sterile inflammation following cell death, but the relative contribution of specific DAMPs, including high-mobility group box 1 (HMGB1), is ill defined. Due to the postnatal lethality of Hmgb7-knockout mice, the role of HMGB1 in sterile inflammation and disease processes in vivo remains controversial. Here, using conditional ablation strategies, we have demonstrated that epithelial, but not bone marrow-derived, HMGB1 is required for sterile inflammation following injury. Epithelial HMGB1, through its receptor RAGE, triggered recruitment of neutrophils, but not macrophages, toward necrosis. In clinically relevant models of necrosis, HMGB1/RAGE-induced neutrophil recruitment mediated subsequent amplification of injury, depending on the presence of neutrophil elastase. Notably, hepatocyte-specific HMGB1 ablation resulted in 100% survival following lethal acetaminophen intoxication. In contrast to necrosis, HMGB1 ablation did not alter inflammation or mortality in response to TNF- or FAS-mediated apoptosis. In LPS-induced shock, in which HMGB1 was considered a key mediator, HMGB1 ablation did not ameliorate inflammation or lethality, despite efficient reduction of HMGB1 serum levels. Our study establishes HMGB1 as a bona fide and targetable DAMP that selectively triggers a neutrophil-mediated injury amplification loop in the setting of necrosis., Introduction Inflammation is a key contributor to many disease processes. Whereas ligand-receptor systems regulating microbial-induced inflammation have been characterized in detail in the past 2 decades, the molecular regulation of [...]

Published
2015
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8. Integrative study of diet-induced mouse models of NAFLD identifies PPARα as a sexually dimorphic drug target

Author

Smati, Sarra, primary, Polizzi, Arnaud, additional, Fougerat, Anne, additional, Ellero-Simatos, Sandrine, additional, Blum, Yuna, additional, Lippi, Yannick, additional, Régnier, Marion, additional, Laroyenne, Alexia, additional, Huillet, Marine, additional, Arif, Muhammad, additional, Zhang, Cheng, additional, Lasserre, Frederic, additional, Marrot, Alain, additional, Al Saati, Talal, additional, Wan, JingHong, additional, Sommer, Caroline, additional, Naylies, Claire, additional, Batut, Aurelie, additional, Lukowicz, Celine, additional, Fougeray, Tiffany, additional, Tramunt, Blandine, additional, Dubot, Patricia, additional, Smith, Lorraine, additional, Bertrand-Michel, Justine, additional, Hennuyer, Nathalie, additional, Pradere, Jean-Philippe, additional, Staels, Bart, additional, Burcelin, Remy, additional, Lenfant, Françoise, additional, Arnal, Jean-François, additional, Levade, Thierry, additional, Gamet-Payrastre, Laurence, additional, Lagarrigue, Sandrine, additional, Loiseau, Nicolas, additional, Lotersztajn, Sophie, additional, Postic, Catherine, additional, Wahli, Walter, additional, Bureau, Christophe, additional, Guillaume, Maeva, additional, Mardinoglu, Adil, additional, Montagner, Alexandra, additional, Gourdy, Pierre, additional, and Guillou, Hervé, additional

Published
2021
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12. HMGB1 links chronic liver injury to progenitor responses and hepatocarcinogenesis

Author

Hernandez, Celine, Huebener, Peter, Pradere, Jean-Philippe, Antoine, Daniel J., Friedman, Richard A., and Schwabe, Robert F.

Subjects
Health care industry
Abstract

The Editors posted an Expression of Concern for this article following notification that an investigative committee at the University of Liverpool had data integrity concerns regarding the mass spectrometry data [...]

Published
2019
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13. The HMGB1/RAGE axis triggers neutrophil-mediated injury amplification following necrosis

Author

Huebener, Peter, Pradere, Jean-Philippe, Hernandez, Celine, Gwak, Geum-Youn, Caviglia, Jorge Matias, Mu, Xueru, Loike, John D., Jenkins, Rosalind E., Antoine, Daniel J., and Schwabe, Robert F.

Subjects
Health care industry
Abstract

An investigative committee at the University of Liverpool recently identified evidence of data fabrication relating to the mass spectrometry data contributed by Daniel J. Antoine for Supplemental Figure 6 of [...]

Published
2019
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14. Integrative study of diet-induced mouse models of NAFLD identifies PPARα as a sexually dimorphic drug target

Author

Smati, Sarra, Polizzi, Arnaud, Fougerat, Anne, Ellero-Simatos, Sandrine, Blum, Yuna, Lippi, Yannick, Régnier, Marion, Laroyenne, Alexia, Huillet, Marine, Arif, Muhammad, Zhang, Cheng, Lasserre, Frederic, Marrot, Alain, Al Saati, Talal, Wan, JingHong, Sommer, Caroline, Naylies, Claire, Batut, Aurelie, Lukowicz, Celine, Fougeray, Tiffany, Tramunt, Blandine, Dubot, Patricia, Smith, Lorraine, Bertrand-Michel, Justine, Hennuyer, Nathalie, Pradere, Jean-Philippe, Staels, Bart, Burcelin, Remy, Lenfant, Francoise, Arnal, Jean-Francois, Levade, Thierry, Gamet-Payrastre, Laurence, Lagarrigue, Sandrine, Loiseau, Nicolas, Lotersztajn, Sophie, Postic, Catherine, Wahli, Walter, Bureau, Christophe, Guillaume, Maeva, Mardinoglu, Adil, Montagner, Alexandra, Gourdy, Pierre, and Guillou, Hervé

Abstract

ObjectiveWe evaluated the influence of sex on the pathophysiology of non-alcoholic fatty liver disease (NAFLD). We investigated diet-induced phenotypic responses to define sex-specific regulation between healthy liver and NAFLD to identify influential pathways in different preclinical murine models and their relevance in humans.DesignDifferent models of diet-induced NAFLD (high-fat diet, choline-deficient high-fat diet, Western diet or Western diet supplemented with fructose and glucose in drinking water) were compared with a control diet in male and female mice. We performed metabolic phenotyping, including plasma biochemistry and liver histology, untargeted large-scale approaches (liver metabolome, lipidome and transcriptome), gene expression profiling and network analysis to identify sex-specific pathways in the mouse liver.ResultsThe different diets induced sex-specific responses that illustrated an increased susceptibility to NAFLD in male mice. The most severe lipid accumulation and inflammation/fibrosis occurred in males receiving the high-fat diet and Western diet, respectively. Sex-biased hepatic gene signatures were identified for these different dietary challenges. The peroxisome proliferator-activated receptor α (PPARα) co-expression network was identified as sexually dimorphic, and in vivo experiments in mice demonstrated that hepatocyte PPARα determines a sex-specific response to fasting and treatment with pemafibrate, a selective PPARα agonist. Liver molecular signatures in humans also provided evidence of sexually dimorphic gene expression profiles and the sex-specific co-expression network for PPARα.ConclusionsThese findings underscore the sex specificity of NAFLD pathophysiology in preclinical studies and identify PPARα as a pivotal, sexually dimorphic, pharmacological target.Trial registration numberNCT02390232.

Published
2022
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21. 336 Gremlin 1 Defines a Mesenchymal Stem Cell in the Gastrointestinal Tract, Bone and Tumor Microenvironment

Author

Worthley, Daniel L., primary, Si, Yiling, additional, Churchill, Michael, additional, Asfaha, Samuel, additional, Manieri, Nicholas, additional, Westphalen, Christoph B., additional, Tailor, Yagnesh H., additional, Hayakawa, Yoku, additional, Carpenter, Jared, additional, Nair, Abhinav, additional, Jin, Guang, additional, Quante, Michael, additional, Glaire, Mark A., additional, Renz, Bernhard W., additional, Pradere, Jean-Philippe, additional, Troeger, Juliane S., additional, Spurrier, Ryan, additional, Levin, Daniel E., additional, Schwabe, Robert, additional, Grikscheit, Tracy, additional, Stappenbeck, Thaddeus S., additional, Mukherjee, Siddhartha, additional, and Wang, Timothy C., additional

Published
2013
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25. 535 JNK1, But Not JNK2 Promotes Hepatic Fibrogenesis

Author

Kluwe, Johannes, primary, Pradere, Jean-Philippe, additional, De Minicis, Samuele, additional, Oesterreicher, Christoph, additional, Mencin, Ali A., additional, Ables, Eleanore, additional, Bataller, Ramon, additional, and Schwabe, Robert F., additional

Published
2009
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26. Promotion of Hepatocellular Carcinoma by the Intestinal Microbiota and TLR4

Author

Bataller, Ramon, Rabadan, Raul, Gwak, Geum Youn, Caviglia, Jorge M., Jang, Myoung Kuk, Bower, Maureen, Khiabanian, Hossein, Pradere, Jean Philippe, Friedman, Richard, Mencin, Ali, Sartor, R. Balfour, Dapito, Dianne H., Mederacke, Ingmar, Lefkowitch, Jay H., Schwabe, Robert F., and Adeyemi, Adebowale

Subjects
digestive system diseases, 3. Good health
Abstract

Increased translocation of intestinal bacteria is a hallmark of chronic liver disease and contributes to hepatic inflammation and fibrosis. Here we tested the hypothesis that the intestinal microbiota and Toll-like receptors (TLRs) promote hepatocellular carcinoma (HCC), a long-term consequence of chronic liver injury, inflammation and fibrosis. Hepatocarcinogenesis in chronically injured livers depended on the intestinal microbiota, and TLR4 activation in non-bone marrow-derived resident liver cells. TLR4 and the intestinal microbiota were not required for HCC initiation but for HCC promotion, mediating increased proliferation, expression of the hepatomitogen epiregulin, and prevention of apoptosis. Gut sterilization restricted to late stages of hepatocarcinogenesis reduced HCC suggesting that the intestinal microbiota and TLR4 represent therapeutic targets for HCC prevention in advanced liver disease.

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