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1. Dysfunctional VLDL metabolism in MASLD.

Author

Marigorta, Urko, Millet, Oscar, Lu, Shelly, and Mato, José

Subjects
Hepatology, Liver diseases, Metabolomics
Abstract

Lipidomics has unveiled the intricate human lipidome, emphasizing the extensive diversity within lipid classes in mammalian tissues critical for cellular functions. This diversity poses a challenge in maintaining a delicate balance between adaptability to recurring physiological changes and overall stability. Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD), linked to factors such as obesity and diabetes, stems from a compromise in the structural and functional stability of the liver within the complexities of lipid metabolism. This compromise inaccurately senses an increase in energy status, such as during fasting-feeding cycles or an upsurge in lipogenesis. Serum lipidomic studies have delineated three distinct metabolic phenotypes, or metabotypes in MASLD. MASLD-A is characterized by lower very low-density lipoprotein (VLDL) secretion and triglyceride (TG) levels, associated with a reduced risk of cardiovascular disease (CVD). In contrast, MASLD-C exhibits increased VLDL secretion and TG levels, correlating with elevated CVD risk. An intermediate subtype, with a blend of features, is designated as the MASLD-B metabotype. In this perspective, we examine into recent findings that show the multifaceted regulation of VLDL secretion by S-adenosylmethionine, the primary cellular methyl donor. Furthermore, we explore the differential CVD and hepatic cancer risk across MASLD metabotypes and discuss the context and potential paths forward to gear the findings from genetic studies towards a better understanding of the observed heterogeneity in MASLD.

Published
2024

2. MetSCORE: a molecular metric to evaluate the risk of metabolic syndrome based on serum NMR metabolomics

Author

Gil-Redondo, Rubén, Conde, Ricardo, Bruzzone, Chiara, Seco, Maria Luisa, Bizkarguenaga, Maider, González-Valle, Beatriz, de Diego, Angela, Laín, Ana, Habisch, Hansjörg, Haudum, Christoph, Verheyen, Nicolas, Obermayer-Pietsch, Barbara, Margarita, Sara, Pelusi, Serena, Verde, Ignacio, Oliveira, Nádia, Sousa, Adriana, Zabala-Letona, Amaia, Santos-Martin, Aida, Loizaga-Iriarte, Ana, Unda-Urzaiz, Miguel, Kazenwadel, Jasmin, Berezhnoy, Georgy, Geisler, Tobias, Gawaz, Meinrad, Cannet, Claire, Schäfer, Hartmut, Diercks, Tammo, Trautwein, Christoph, Carracedo, Arkaitz, Madl, Tobias, Valenti, Luca, Spraul, Manfred, Lu, Shelly C., Embade, Nieves, Mato, José M., and Millet, Oscar

Published
2024
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4. Metabolic subtypes of patients with NAFLD exhibit distinctive cardiovascular risk profiles

Author

Martínez‐Arranz, Ibon, Bruzzone, Chiara, Noureddin, Mazen, Gil‐Redondo, Ruben, Mincholé, Itziar, Bizkarguenaga, Maider, Arretxe, Enara, Iruarrizaga‐Lejarreta, Marta, Fernández‐Ramos, David, Lopitz‐Otsoa, Fernando, Mayo, Rebeca, Embade, Nieves, Newberry, Elizabeth, Mittendorf, Bettina, Izquierdo‐Sánchez, Laura, Smid, Vaclav, Arnold, Jorge, Iruzubieta, Paula, Castaño, Ylenia Pérez, Krawczyk, Marcin, Marigorta, Urko M, Morrison, Martine C, Kleemann, Robert, Martín‐Duce, Antonio, Hayardeny, Liat, Vitek, Libor, Bruha, Radan, de la Fuente, Rocío Aller, Crespo, Javier, Romero‐Gomez, Manuel, Banales, Jesus M, Arrese, Marco, Cusi, Kenneth, Bugianesi, Elisabetta, Klein, Samuel, Lu, Shelly C, Anstee, Quentin M, Millet, Oscar, Davidson, Nicholas O, Alonso, Cristina, and Mato, José M

Subjects
Medical Biochemistry and Metabolomics, Biomedical and Clinical Sciences, Heart Disease, Cardiovascular, Chronic Liver Disease and Cirrhosis, Digestive Diseases, Genetics, Liver Disease, Atherosclerosis, Clinical Research, Aetiology, 2.1 Biological and endogenous factors, Good Health and Well Being, Animals, Apolipoproteins B, Cardiovascular Diseases, Cholesterol, VLDL, Heart Disease Risk Factors, Lipoproteins, VLDL, Liver, Mice, Non-alcoholic Fatty Liver Disease, Phospholipases, Risk Factors, Triglycerides, Clinical Sciences, Immunology, Gastroenterology & Hepatology, Clinical sciences
Abstract

Background and aimsWe previously identified subsets of patients with NAFLD with different metabolic phenotypes. Here we align metabolomic signatures with cardiovascular disease (CVD) and genetic risk factors.Approach and resultsWe analyzed serum metabolome from 1154 individuals with biopsy-proven NAFLD, and from four mouse models of NAFLD with impaired VLDL-triglyceride (TG) secretion, and one with normal VLDL-TG secretion. We identified three metabolic subtypes: A (47%), B (27%), and C (26%). Subtype A phenocopied the metabolome of mice with impaired VLDL-TG secretion; subtype C phenocopied the metabolome of mice with normal VLDL-TG; and subtype B showed an intermediate signature. The percent of patients with NASH and fibrosis was comparable among subtypes, although subtypes B and C exhibited higher liver enzymes. Serum VLDL-TG levels and secretion rate were lower among subtype A compared with subtypes B and C. Subtype A VLDL-TG and VLDL-apolipoprotein B concentrations were independent of steatosis, whereas subtypes B and C showed an association with these parameters. Serum TG, cholesterol, VLDL, small dense LDL5,6 , and remnant lipoprotein cholesterol were lower among subtype A compared with subtypes B and C. The 10-year high risk of CVD, measured with the Framingham risk score, and the frequency of patatin-like phospholipase domain-containing protein 3 NAFLD risk allele were lower in subtype A.ConclusionsMetabolomic signatures identify three NAFLD subgroups, independent of histological disease severity. These signatures align with known CVD and genetic risk factors, with subtype A exhibiting a lower CVD risk profile. This may account for the variation in hepatic versus cardiovascular outcomes, offering clinically relevant risk stratification.

Published
2022

5. Characterization of preovulatory follicular fluid secretome and its effects on equine oocytes during in vitro maturation

Author

Luis-Calero, Marcos, Marinaro, Federica, Fernández-Hernández, Pablo, Ortiz-Rodríguez, José M., G. Casado, Javier, Pericuesta, Eva, Gutiérrez-Adán, Alfonso, González, Esperanza, Azkargorta, Mikel, Conde, Ricardo, Bizkarguenaga, Maider, Embade, Nieves, Elortza, Félix, Falcón-Pérez, Juan M., Millet, Óscar, González-Fernández, Lauro, and Macías-García, Beatriz

Published
2024
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6. Depletion of mitochondrial methionine adenosyltransferase α1 triggers mitochondrial dysfunction in alcohol-associated liver disease

Author

Barbier-Torres, Lucía, Murray, Ben, Yang, Jin Won, Wang, Jiaohong, Matsuda, Michitaka, Robinson, Aaron, Binek, Aleksandra, Fan, Wei, Fernández-Ramos, David, Lopitz-Otsoa, Fernando, Luque-Urbano, Maria, Millet, Oscar, Mavila, Nirmala, Peng, Hui, Ramani, Komal, Gottlieb, Roberta, Sun, Zhaoli, Liangpunsakul, Suthat, Seki, Ekihiro, Van Eyk, Jennifer E, Mato, Jose M, and Lu, Shelly C

Subjects
Biochemistry and Cell Biology, Biological Sciences, Substance Misuse, Liver Disease, Chronic Liver Disease and Cirrhosis, Alcoholism, Alcohol Use and Health, Digestive Diseases, Aetiology, 2.1 Biological and endogenous factors, Oral and gastrointestinal, Good Health and Well Being, Animals, Blotting, Western, Casein Kinase II, Cell Line, Ethanol, Female, Hep G2 Cells, Hepatocytes, Humans, Isoenzymes, Liver, Liver Diseases, Alcoholic, Methionine Adenosyltransferase, Mice, Inbred C57BL, Mitochondria, Mitochondrial Proteins, Mutation, NIMA-Interacting Peptidylprolyl Isomerase, Protein Binding
Abstract

MATα1 catalyzes the synthesis of S-adenosylmethionine, the principal biological methyl donor. Lower MATα1 activity and mitochondrial dysfunction occur in alcohol-associated liver disease. Besides cytosol and nucleus, MATα1 also targets the mitochondria of hepatocytes to regulate their function. Here, we show that mitochondrial MATα1 is selectively depleted in alcohol-associated liver disease through a mechanism that involves the isomerase PIN1 and the kinase CK2. Alcohol activates CK2, which phosphorylates MATα1 at Ser114 facilitating interaction with PIN1, thereby inhibiting its mitochondrial localization. Blocking PIN1-MATα1 interaction increased mitochondrial MATα1 levels and protected against alcohol-induced mitochondrial dysfunction and fat accumulation. Normally, MATα1 interacts with mitochondrial proteins involved in TCA cycle, oxidative phosphorylation, and fatty acid β-oxidation. Preserving mitochondrial MATα1 content correlates with higher methylation and expression of mitochondrial proteins. Our study demonstrates a role of CK2 and PIN1 in reducing mitochondrial MATα1 content leading to mitochondrial dysfunction in alcohol-associated liver disease.

Published
2022

7. Prospective Metabolomic Studies in Precision Medicine: The AKRIBEA Project

Author

Bizkarguenaga, Maider, Gil-Redondo, Rubén, Bruzzone, Chiara, Bernardo-Seisdedos, Ganeko, Laín, Ana, González-Valle, Beatriz, Embade, Nieves, Mato, José M., Millet, Oscar, Michel, Martin C., Editor-in-Chief, Barrett, James E., Editorial Board Member, Centurión, David, Editorial Board Member, Flockerzi, Veit, Editorial Board Member, Geppetti, Pierangelo, Editorial Board Member, Hofmann, Franz B., Editorial Board Member, Meier, Kathryn Elaine, Editorial Board Member, Page, Clive P., Editorial Board Member, Wang, KeWei, Editorial Board Member, Ghini, Veronica, editor, Stringer, Kathleen A., editor, and Luchinat, Claudio, editor

Published
2023
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9. Hepatocyte-specific O-GlcNAc transferase downregulation ameliorates nonalcoholic steatohepatitis by improving mitochondrial function

Author

Gonzalez-Rellan, Maria J., Parracho, Tamara, Heras, Violeta, Rodriguez, Amaia, Fondevila, Marcos F., Novoa, Eva, Lima, Natalia, Varela-Rey, Marta, Senra, Ana, Chantada-Vazquez, Maria D.P., Ameneiro, Cristina, Bernardo, Ganeko, Fernandez-Ramos, David, Lopitz-Otsoa, Fernando, Bilbao, Jon, Guallar, Diana, Fidalgo, Miguel, Bravo, Susana, Dieguez, Carlos, Martinez-Chantar, Maria L., Millet, Oscar, Mato, Jose M., Schwaninger, Markus, Prevot, Vincent, Crespo, Javier, Frühbeck, Gema, Iruzubieta, Paula, and Nogueiras, Ruben

Published
2023
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10. Hepatic levels of S-adenosylmethionine regulate the adaptive response to fasting

Author

Capelo-Diz, Alba, Lachiondo-Ortega, Sofía, Fernández-Ramos, David, Cañas-Martín, Jorge, Goikoetxea-Usandizaga, Naroa, Serrano-Maciá, Marina, González-Rellan, Maria J., Mosca, Laura, Blazquez-Vicens, Joan, Tinahones-Ruano, Alberto, Fondevila, Marcos F., Buyan, Mason, Delgado, Teresa C., Gutierrez de Juan, Virginia, Ayuso-García, Paula, Sánchez-Rueda, Alejandro, Velasco-Avilés, Sergio, Fernández-Susavila, Héctor, Riobello-Suárez, Cristina, Dziechciarz, Bartlomiej, Montiel-Duarte, Cristina, Lopitz-Otsoa, Fernando, Bizkarguenaga, Maider, Bilbao-García, Jon, Bernardo-Seisdedos, Ganeko, Senra, Ana, Soriano-Navarro, Mario, Millet, Oscar, Díaz-Lagares, Ángel, Crujeiras, Ana B., Bao-Caamano, Aida, Cabrera, Diana, van Liempd, Sebastiaan, Tamayo-Caro, Miguel, Borzacchiello, Luigi, Gomez-Santos, Beatriz, Buqué, Xabier, Sáenz de Urturi, Diego, González-Romero, Francisco, Simon, Jorge, Rodríguez-Agudo, Rubén, Ruiz, Asier, Matute, Carlos, Beiroa, Daniel, Falcon-Perez, Juan M., Aspichueta, Patricia, Rodríguez-Cuesta, Juan, Porcelli, Marina, Pajares, María A., Ameneiro, Cristina, Fidalgo, Miguel, Aransay, Ana M., Lama-Díaz, Tomas, Blanco, Miguel G., López, Miguel, Villa-Bellosta, Ricardo, Müller, Timo D., Nogueiras, Rubén, Woodhoo, Ashwin, Martínez-Chantar, María Luz, and Varela-Rey, Marta

Published
2023
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11. Performance of non-invasive tests and histology for the prediction of clinical outcomes in patients with non-alcoholic fatty liver disease: an individual participant data meta-analysis

Author

Anstee, Quentin M, Daly, Ann K, Govaere, Olivier, Cockell, Simon, Tiniakos, Dina, Bedossa, Pierre, Burt, Alastair, Oakley, Fiona, Cordell, Heather J, Day, Christopher P, Wonders, Kristy, Missier, Paolo, McTeer, Matthew, Vale, Luke, Oluboyede, Yemi, Breckons, Matt, Bossuyt, Patrick M, Zafarmand, Hadi, Vali, Yasaman, Lee, Jenny, Nieuwdorp, Max, Holleboom, Adriaan G, Verheij, Joanne, Ratziu, Vlad, Clément, Karine, Patino-Navarrete, Rafael, Pais, Raluca, Paradis, Valerie, Schuppan, Detlef, Schattenberg, Jörn M, Surabattula, Rambabu, Myneni, Sudha, Straub, Beate K, Vidal-Puig, Toni, Vacca, Michele, Rodrigues-Cuenca, Sergio, Allison, Mike, Kamzolas, Ioannis, Petsalaki, Evangelia, Campbell, Mark, Lelliott, Chris J, Davies, Susan, Orešič, Matej, Hyötyläinen, Tuulia, McGlinchey, Aiden, Mato, Jose M, Millet, Óscar, Dufour, Jean-François, Berzigotti, Annalisa, Masoodi, Mojgan, Pavlides, Michael, Harrison, Stephen, Neubauer, Stefan, Cobbold, Jeremy, Mozes, Ferenc, Akhtar, Salma, Olodo-Atitebi, Seliat, Banerjee, Rajarshi, Kelly, Matt, Shumbayawonda, Elizabeth, Dennis, Andrea, Andersson, Anneli, Wigley, Ioan, Romero-Gómez, Manuel, Gómez-González, Emilio, Ampuero, Javier, Castell, Javier, Gallego-Durán, Rocío, Fernández, Isabel, Montero-Vallejo, Rocío, Karsdal, Morten, Rasmussen, Daniel Guldager Kring, Leeming, Diana Julie, Sinisi, Antonia, Musa, Kishwar, Sandt, Estelle, Tonini, Manuela, Bugianesi, Elisabetta, Rosso, Chiara, Armandi, Angelo, Marra, Fabio, Gastaldelli, Amalia, Svegliati, Gianluca, Boursier, Jérôme, Francque, Sven, Vonghia, Luisa, Driessen, Ann, Ekstedt, Mattias, Kechagias, Stergios, Yki-Järvinen, Hannele, Porthan, Kimmo, Arola, Johanna, van Mil, Saskia, Papatheodoridis, George, Cortez-Pinto, Helena, Rodrigues, Cecilia M P, Valenti, Luca, Pelusi, Serena, Petta, Salvatore, Pennisi, Grazia, Miele, Luca, Geier, Andreas, Trautwein, Christian, Reißing, Johanna, Aithal, Guruprasad P, Francis, Susan, Palaniyappan, Naaventhan, Bradley, Christopher, Hockings, Paul, Schneider, Moritz, Newsome, Philip, Hübscher, Stefan, Wenn, David, Rosenquist, Christian, Trylesinski, Aldo, Mayo, Rebeca, Alonso, Cristina, Duffin, Kevin, Perfield, James W, Chen, Yu, Yunis, Carla, Tuthill, Theresa, Harrington, Magdalena Alicia, Miller, Melissa, Chen, Yan, McLeod, Euan James, Ross, Trenton, Bernardo, Barbara, Schölch, Corinna, Ertle, Judith, Younes, Ramy, Oldenburger, Anouk, Coxson, Harvey, Ostroff, Rachel, Alexander, Leigh, Biegel, Hannah, Kjær, Mette Skalshøi, Harder, Lea Mørch, Davidsen, Peter, Ellegaard, Jens, Balp, Maria-Magdalena, Brass, Clifford, Jennings, Lori, Martic, Miljen, Löffler, Jürgen, Applegate, Douglas, Shankar, Sudha, Torstenson, Richard, Lindén, Daniel, Fournier-Poizat, Céline, Llorca, Anne, Kalutkiewicz, Michael, Pepin, Kay, Ehman, Richard, Horan, Gerald, Ho, Gideon, Tai, Dean, Chng, Elaine, Patterson, Scott D, Billin, Andrew, Doward, Lynda, Twiss, James, Thakker, Paresh, Derdak, Zoltan, Landgren, Henrik, Lackner, Carolin, Gouw, Annette, Hytiroglou, Prodromos, Mózes, Ferenc E, Lee, Jenny A, Alzoubi, Osama, Staufer, Katharina, Trauner, Michael, Paternostro, Rafael, Stauber, Rudolf E, van Dijk, Anne-Marieke, Mak, Anne Linde, de Saint Loup, Marc, Shima, Toshihide, Gaia, Silvia, Shalimar, Lupșor-Platon, Monica, Wong, Vincent Wai-Sun, Li, Guanlin, Wong, Grace Lai-Hung, Karlas, Thomas, Wiegand, Johannes, Sebastiani, Giada, Tsochatzis, Emmanuel, Liguori, Antonio, Yoneda, Masato, Nakajima, Atsushi, Hagström, Hannes, Akbari, Camilla, Hirooka, Masashi, Chan, Wah-Kheong, Mahadeva, Sanjiv, Rajaram, Ruveena, Zheng, Ming-Hua, George, Jacob, Eslam, Mohammed, Viganò, Mauro, Ridolfo, Sofia, Aithal, Guruprasad Padur, Lee, Dae Ho, Nasr, Patrik, Cassinotto, Christophe, de Lédinghen, Victor, Mendoza, Yuly P, Noureddin, Mazen, Truong, Emily, and Harrison, Stephen A

Published
2023
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12. SARS-CoV-2 Infection Dysregulates the Metabolomic and Lipidomic Profiles of Serum.

Author

Bruzzone, Chiara, Bizkarguenaga, Maider, Gil-Redondo, Rubén, Diercks, Tammo, Arana, Eunate, García de Vicuña, Aitor, Seco, Marisa, Bosch, Alexandre, Palazón, Asís, San Juan, Itxaso, Laín, Ana, Gil-Martínez, Jon, Bernardo-Seisdedos, Ganeko, Fernández-Ramos, David, Lopitz-Otsoa, Fernando, Embade, Nieves, Lu, Shelly, Mato, José M, and Millet, Oscar

Subjects
Human Metabolism, Metabolomics, Virology
Abstract

COVID-19 is a systemic infection that exerts significant impact on the metabolism. Yet, there is little information on how SARS-CoV-2 affects metabolism. Using NMR spectroscopy, we measured the metabolomic and lipidomic serum profile from 263 (training cohort) + 135 (validation cohort) symptomatic patients hospitalized after positive PCR testing for SARS-CoV-2 infection. We also established the profiles of 280 persons collected before the coronavirus pandemic started. Principal-component analysis discriminated both cohorts, highlighting the impact that the infection has on overall metabolism. The lipidomic analysis unraveled a pathogenic redistribution of the lipoprotein particle size and composition to increase the atherosclerotic risk. In turn, metabolomic analysis reveals abnormally high levels of ketone bodies (acetoacetic acid, 3-hydroxybutyric acid, and acetone) and 2-hydroxybutyric acid, a readout of hepatic glutathione synthesis and marker of oxidative stress. Our results are consistent with a model in which SARS-CoV-2 infection induces liver damage associated with dyslipidemia and oxidative stress.

Published
2020

14. Hyperphosphorylation of hepatic proteome characterizes nonalcoholic fatty liver disease in S-adenosylmethionine deficiency

Author

Robinson, Aaron E., Binek, Aleksandra, Ramani, Komal, Sundararaman, Niveda, Barbier-Torres, Lucía, Murray, Ben, Venkatraman, Vidya, Kreimer, Simion, Ardle, Angela Mc, Noureddin, Mazen, Fernández-Ramos, David, Lopitz-Otsoa, Fernando, Gutiérrez de Juan, Virginia, Millet, Oscar, Mato, José M., Lu, Shelly C., and Van Eyk, Jennifer E.

Published
2023
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19. Increased serum miR-193a-5p during non-alcoholic fatty liver disease progression: Diagnostic and mechanistic relevance

Author

Clark, James, Cordell, Heather J., Darlay, Rebecca, Day, Christopher P., Hardy, Tim, Liu, Yang-Lin, Oakley, Fiona, Palmer, Jeremy, Queen, Rachel, Wonders, Kristy, Bossuyt, Patrick M., Holleboom, Adriaan G., Zafarmand, Hadi, Vali, Yasaman, Lee, Jenny, Clement, Karine, Pais, Raluca, Schuppan, Detlef, Allison, Michael, Cuenca, Sergio Rodriguez, Pellegrinelli, Vanessa, Vacca, Michele, Vidal-Puig, Antonio, Hyötyläinen, Tuulia, McGlinchey, Aidan, Orešič, Matej, Sen, Partho, Mato, Jose, Millet, Óscar, Dufour, Jean-Francois, Harrison, Stephen, Neubauer, Stefan, Pavlides, Michael, Mozes, Ferenc, Akhtar, Salma, Banerjee, Rajarshi, Kelly, Matt, Shumbayawonda, Elizabeth, Dennis, Andrea, Erpicum, Charlotte, Romero-Gomez, Manuel, Gallego-Durán, Rocío, Fernández, Isabel, Karsdal, Morten, Leeming, Diana, Fisker, Mette Juul, Erhardtsen, Elisabeth, Rasmussen, Daniel, Qvist, Per, Sinisi, Antonia, Sandt, Estelle, Tonini, Maria Manuela, Parola, Maurizio, Rosso, Chiara, Marra, Fabio, Gastaldelli, Amalia, Francque, Sven, Kechagias, Stergios, Yki-Järvinen, Hannele, Porthan, Kimmo, van Mil, Saskia, Papatheodoridis, George, Cortez-Pinto, Helena, Valenti, Luca, Petta, Salvatore, Miele, Luca, Geier, Andreas, Trautwein, Christian, Hockings, Paul, Newsome, Phil, Wenn, David, Pereira Rodrigues, Cecília Maria, Hanf, Rémy, Chaumat, Pierre, Rosenquist, Christian, Trylesinski, Aldo, Ortiz, Pablo, Duffin, Kevin, Yunis, Carla, Miller, Melissa, Tuthill, Theresa, Ertle, Judith, Younes, Ramy, Alexander, Leigh, Ostroff, Rachel, Kjær, Mette Skalshøi, Mikkelsen, Lars Friis, Brass, Clifford, Jennings, Lori, Balp, Maria-Magdalena, Martic, Miljen, Hanauer, Guido, Shankar, Sudha, Torstenson, Richard, Fournier, Céline, Ehman, Richard, Kalutkiewicz, Michael, Pepin, Kay, Myers, Joel, Shevell, Diane, Ho, Gideon, Landgren, Henrik, Myers, Rob, Doward, Lynda, Whalley, Diane, Twiss, James, Johnson, Katherine, Leary, Peter J., Govaere, Olivier, Barter, Matthew J., Charlton, Sarah H., Cockell, Simon J., Tiniakos, Dina, Zatorska, Michalina, Bedossa, Pierre, Brosnan, M. Julia, Cobbold, Jeremy F., Ekstedt, Mattias, Aithal, Guruprasad P., Clément, Karine, Schattenberg, Jörn M., Boursier, Jerome, Ratziu, Vlad, Bugianesi, Elisabetta, Anstee, Quentin M., and Daly, Ann K.

Published
2022
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20. Pseudophosphorylation of single residues of the J‐domain of DNAJA2 regulates the holding/folding balance of the Hsc70 system.

Author

Velasco‐Carneros, Lorea, Bernardo‐Seisdedos, Ganeko, Maréchal, Jean‐Didier, Millet, Oscar, Moro, Fernando, and Muga, Arturo

Abstract

The Hsp70 system is essential for maintaining protein homeostasis and comprises a central Hsp70 and two accessory proteins that belong to the J‐domain protein (JDP) and nucleotide exchange factor families. Posttranslational modifications offer a means to tune the activity of the system. We explore how phosphorylation of specific residues of the J‐domain of DNAJA2, a class A JDP, regulates Hsc70 activity using biochemical and structural approaches. Among these residues, we find that pseudophosphorylation of Y10 and S51 enhances the holding/folding balance of the Hsp70 system, reducing cochaperone collaboration with Hsc70 while maintaining the holding capacity. Truly phosphorylated J domains corroborate phosphomimetic variant effects. Notably, distinct mechanisms underlie functional impacts of these DNAJA2 variants. Pseudophosphorylation of Y10 induces partial disordering of the J domain, whereas the S51E substitution weakens essential DNAJA2‐Hsc70 interactions without a large structural reorganization of the protein. S51 phosphorylation might be class‐specific, as all cytosolic class A human JDPs harbor a phosphorylatable residue at this position. [ABSTRACT FROM AUTHOR]

Published
2024
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22. Cross-Validation of Metabolic Phenotypes in SARS-CoV-2 Infected Subpopulations Using Targeted Liquid Chromatography–Mass Spectrometry (LC-MS)

Author

Whiley, Luke, primary, Lawler, Nathan G., additional, Zeng, Annie Xu, additional, Lee, Alex, additional, Chin, Sung-Tong, additional, Bizkarguenaga, Maider, additional, Bruzzone, Chiara, additional, Embade, Nieves, additional, Wist, Julien, additional, Holmes, Elaine, additional, Millet, Oscar, additional, Nicholson, Jeremy K., additional, and Gray, Nicola, additional

Published
2024
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26. A molecular signature for the metabolic syndrome by urine metabolomics

Author

Bruzzone, Chiara, Gil-Redondo, Rubén, Seco, Marisa, Barragán, Rocío, de la Cruz, Laura, Cannet, Claire, Schäfer, Hartmut, Fang, Fang, Diercks, Tammo, Bizkarguenaga, Maider, González-Valle, Beatriz, Laín, Ana, Sanz-Parra, Arantza, Coltell, Oscar, de Letona, Ander López, Spraul, Manfred, Lu, Shelly C., Buguianesi, Elisabetta, Embade, Nieves, Anstee, Quentin M., Corella, Dolores, Mato, José M., and Millet, Oscar

Published
2021
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27. O-GlcNAcylated p53 in the liver modulates hepatic glucose production

Author

Gonzalez-Rellan, Maria J., Fondevila, Marcos F., Fernandez, Uxia, Rodríguez, Amaia, Varela-Rey, Marta, Veyrat-Durebex, Christelle, Seoane, Samuel, Bernardo, Ganeko, Lopitz-Otsoa, Fernando, Fernández-Ramos, David, Bilbao, Jon, Iglesias, Cristina, Novoa, Eva, Ameneiro, Cristina, Senra, Ana, Beiroa, Daniel, Cuñarro, Juan, DP Chantada-Vazquez, Maria, Garcia-Vence, Maria, Bravo, Susana B., Da Silva Lima, Natalia, Porteiro, Begoña, Carneiro, Carmen, Vidal, Anxo, Tovar, Sulay, Müller, Timo D., Ferno, Johan, Guallar, Diana, Fidalgo, Miguel, Sabio, Guadalupe, Herzig, Stephan, Yang, Won Ho, Cho, Jin Won, Martinez-Chantar, Maria Luz, Perez-Fernandez, Roman, López, Miguel, Dieguez, Carlos, Mato, Jose M., Millet, Oscar, Coppari, Roberto, Woodhoo, Ashwin, Fruhbeck, Gema, and Nogueiras, Ruben

Published
2021
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30. Quantitative Analysis of the Human Semen Phosphorometabolome by 31 P-NMR.

Author

Serrano, Rebeca, Martin-Hidalgo, David, Bilbao, Jon, Bernardo-Seisdedos, Ganeko, Millet, Oscar, Garcia-Marin, Luis J., and Bragado, Maria Julia

Subjects
SEMEN analysis, SEMEN, LIPID metabolism, SPERM motility, CARBOHYDRATE metabolism, ENERGY metabolism
Abstract

Phosphorus-containing metabolites occupy a prominent position in cell pathways. The phosphorometabolomic approach in human sperm samples will deliver valuable information as new male fertility biomarkers could emerge. This study analyzed, by 31P-NMR, seminal plasma and whole semen from asthenozoospermic and normozoospermic samples (71% vs. 27% and 45% vs. 17%, total and progressive sperm motility, respectively), and also ejaculates from healthy donors. At least 16 phosphorus-containing metabolites involved in central energy metabolism and phospholipid, nucleotide, and nicotinamide metabolic pathways were assigned and different abundances between the samples with distinct sperm quality was detected. Specifically, higher levels of phosphocholine, glucose-1-phosphate, and to a lesser degree, acetyl phosphate were found in the asthenozoospermic seminal plasma. Notably, the phosphorometabolites implicated in lipid metabolism were highlighted in the seminal plasma, while those associated with carbohydrate metabolism were more abundant in the spermatozoa. Higher levels of phosphocholine, glucose-1-phosphate, and acetyl phosphate in the seminal plasma with poor quality suggest their crucial role in supporting sperm motility through energy metabolic pathways. In the seminal plasma, phosphorometabolites related to lipid metabolism were prominent; however, spermatozoa metabolism is more dependent on carbohydrate-related energy pathways. Understanding the presence and function of sperm phosphorylated metabolites will enhance our knowledge of the metabolic profile of healthy human sperm, improving assessment and differential diagnosis. [ABSTRACT FROM AUTHOR]

Published
2024
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31. Thermodynamic Stabilization of Human Frataxin

Author

Nunez-Franco, Reyes, primary, Torres-Mozas, Angel, additional, Navo, Claudio D., additional, Schedlbauer, Andreas, additional, Azkargorta, Mikel, additional, Iloro, Ibon, additional, Elortza, Felix, additional, Ortega, Gabriel, additional, Millet, Oscar, additional, Peccati, Francesca, additional, and Jimenez-Oses, Gonzalo, additional

Published
2023
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32. Serum and Urine Metabolomic Profiling of Newly Diagnosed Treatment-Naïve Inflammatory Bowel Disease Patients

Author

Aldars-García, Laila, primary, Gil-Redondo, Rubén, additional, Embade, Nieves, additional, Riestra, Sabino, additional, Rivero, Montserrat, additional, Gutiérrez, Ana, additional, Rodríguez-Lago, Iago, additional, Fernández-Salazar, Luis, additional, Ceballos, Daniel, additional, Manuel Benítez, José, additional, Aguas, Mariam, additional, Baston-Rey, Iria, additional, Bermejo, Fernando, additional, José Casanova, María, additional, Lorente, Rufo, additional, Ber, Yolanda, additional, Ginard, Daniel, additional, Esteve, María, additional, de Francisco, Ruth, additional, José García, María, additional, Francés, Rubén, additional, Rodríguez Pescador, Ainhoa, additional, Velayos, Benito, additional, del Río, Elena Guerra, additional, Marín Pedrosa, Sandra, additional, Minguez Sabater, Alejandro, additional, Barreiro-de Acosta, Manuel, additional, Algaba, Alicia, additional, Verdejo Gil, Cristina, additional, Rivas, Olga, additional, Royo, Vanesa, additional, Aceituno, Montserrat, additional, Garre, Ana, additional, Baldán-Martín, Montserrat, additional, Ramírez, Cristina, additional, Sanz-García, Ancor, additional, Lozano, Juan J, additional, Sidorova, Julia, additional, Millet, Oscar, additional, Bernardo, David, additional, Gisbert, Javier P, additional, and Chaparro, María, additional

Published
2023
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34. Contributors

Author

Abian, Olga, primary, Bellezza, Ilaria, additional, Bernardo-Seisdedos, Ganeko, additional, Betancor-Fernandez, Isabel, additional, Blouin, Jean-Marc, additional, Broersen, Kerensa, additional, Calloni, Giulia, additional, Cellini, Barbara, additional, Christensen, Caspar E., additional, Conejero-Lara, Francisco, additional, Cristóvão, Joana S., additional, Flydal, Marte I., additional, Fontana, Nicole, additional, Fowler, Douglas M., additional, Gil, David, additional, Gomes, Cláudio M., additional, Good, Sarah, additional, Grabrucker, Andreas M., additional, Grande, Fedora, additional, Grottelli, Silvia, additional, Hanyaloglu, Aylin C., additional, Hartmann-Petersen, Rasmus, additional, Hausvik, Emil, additional, Janovick, Jo Ann, additional, Jepsen, Michael Maglegaard, additional, Lindorff-Larsen, Kresten, additional, Martinez, Aurora, additional, McCorvie, Thomas J., additional, Millet, Oscar, additional, Moreira, Guilherme G., additional, Morel, Bertrand, additional, Naganathan, Athi N., additional, Neira, Jose L., additional, Nielsen, Sofie V., additional, Pey, Angel L., additional, Richard, Emmanuel, additional, Rizzuti, Bruno, additional, Salido, Eduardo, additional, Schenstrøm, Signe M., additional, Støve, Svein I., additional, Stein, Amelie, additional, Timson, David J., additional, Ulloa-Aguirre, Alfredo, additional, Underhaug, Jarl, additional, Vabulas, R. Martin, additional, van Oosten-Hawle, Patricija, additional, Vega, Sonia, additional, Velazquez-Campoy, Adrian, additional, Yue, Wyatt W., additional, and Zariñán, Teresa, additional

Published
2020
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36. Integrative Plasma Metabolic and Lipidomic Modelling of SARS-CoV-2 Infection in Relation to Clinical Severity and Early Mortality Prediction

Author

Lodge, Samantha, primary, Lawler, Nathan G., additional, Gray, Nicola, additional, Masuda, Reika, additional, Nitschke, Philipp, additional, Whiley, Luke, additional, Bong, Sze-How, additional, Yeap, Bu B., additional, Dwivedi, Girish, additional, Spraul, Manfred, additional, Schaefer, Hartmut, additional, Gil-Redondo, Rubén, additional, Embade, Nieves, additional, Millet, Oscar, additional, Holmes, Elaine, additional, Wist, Julien, additional, and Nicholson, Jeremy K., additional

Published
2023
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37. mTORC1 response to glucose via dihydroxyacetone phosphate is regulated by MAT1A. Role in NAFLD

Author

de los Reyes Luque Urbano, María, primary, Bilbao, Jon, additional, Ramos, David Fernández, additional, Otsoa, Fernando Lopitz, additional, de Juan, Virginia Gutiérrez, additional, Bernardo-Seisdedos, Ganeko, additional, Cervera Seco, Luis Manuel, additional, Marigorta, Urko M, additional, Torres, Lucía Barbier, additional, Lu, Shelly C., additional, Millet, Oscar, additional, and Mato, José M., additional

Published
2023
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39. Urinary metabolomic profile of youth at risk for chronic kidney disease in Nicaragua

Author

Hall, Samantha M., primary, Raines, Nathan H., additional, Ramirez-Rubio, Oriana, additional, Amador, Juan José, additional, López-Pilarte, Damaris, additional, O’Callaghan-Gordo, Cristina, additional, Gil-Redondo, Rubén, additional, Embade, Nieves, additional, Millet, Oscar, additional, Peng, Xiaojing, additional, Vences, Selene, additional, Keogh, Sinead A., additional, Delgado, Iris S., additional, Friedman, David J., additional, Brooks, Daniel R., additional, and Leibler, Jessica H., additional

Published
2023
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40. Metabolic Features of Increased Gut Permeability, Inflammation, and Altered Energy Metabolism Distinguish Agricultural Workers at Risk for Mesoamerican Nephropathy

Author

Raines, Nathan H., primary, Leone, Dominick A., additional, O’Callaghan-Gordo, Cristina, additional, Ramirez-Rubio, Oriana, additional, Amador, Juan José, additional, Lopez Pilarte, Damaris, additional, Delgado, Iris S., additional, Leibler, Jessica H., additional, Embade, Nieves, additional, Gil-Redondo, Rubén, additional, Bruzzone, Chiara, additional, Bizkarguenaga, Maider, additional, Scammell, Madeleine K., additional, Parikh, Samir M., additional, Millet, Oscar, additional, Brooks, Daniel R., additional, and Friedman, David J., additional

Published
2023
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41. Redox regulation of KV7 channels through EF3 hand of calmodulin

Author

Nuñez, Eider, primary, Jones, Frederick, additional, Muguruza-Montero, Arantza, additional, Urrutia, Janire, additional, Aguado, Alejandra, additional, Malo, Covadonga, additional, Bernardo-Seisdedos, Ganeko, additional, Domene, Carmen, additional, Millet, Oscar, additional, Gamper, Nikita, additional, and Villarroel, Alvaro, additional

Published
2023
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43. Redox regulation of KV7 channels through EF3 hand of calmodulin

Author

Nuñez, Eider, Jones, Frederick, Muguruza-Montero, Arantza, Urrutia, Janire, Aguado, Alejandra, Malo, Covadonga, Bernardo-Seisdedos, Ganeko, Domene, Carmen, Millet, Oscar, Gamper, Nikita, Villarroel, Alvaro, Nuñez, Eider, Jones, Frederick, Muguruza-Montero, Arantza, Urrutia, Janire, Aguado, Alejandra, Malo, Covadonga, Bernardo-Seisdedos, Ganeko, Domene, Carmen, Millet, Oscar, Gamper, Nikita, and Villarroel, Alvaro

Abstract

Neuronal KV7 channels, important regulators of cell excitability, are among the most sensitive proteins to reactive oxygen species. The S2S3 linker of the voltage sensor was reported as a site-mediating redox modulation of the channels. Recent structural insights reveal potential interactions between this linker and the Ca2+-binding loop of the third EF-hand of calmodulin (CaM), which embraces an antiparallel fork formed by the C-terminal helices A and B, constituting the calcium responsive domain (CRD). We found that precluding Ca2+ binding to the EF3 hand, but not to EF1, EF2, or EF4 hands, abolishes oxidation-induced enhancement of KV7.4 currents. Monitoring FRET (Fluorescence Resonance Energy Transfer) between helices A and B using purified CRDs tagged with fluorescent proteins, we observed that S2S3 peptides cause a reversal of the signal in the presence of Ca2+ but have no effect in the absence of this cation or if the peptide is oxidized. The capacity of loading EF3 with Ca2+ is essential for this reversal of the FRET signal, whereas the consequences of obliterating Ca2+ binding to EF1, EF2, or EF4 are negligible. Furthermore, we show that EF3 is critical for translating Ca2+ signals to reorient the AB fork. Our data are consistent with the proposal that oxidation of cysteine residues in the S2S3 loop relieves KV7 channels from a constitutive inhibition imposed by interactions between the EF3 hand of CaM which is crucial for this signaling.

Published
2023

44. Hepatocyte-specific O-GlcNAc transferase downregulation ameliorates nonalcoholic steatohepatitis by improving mitochondrial function

Author

Universidade de Santiago de Compostela. Centro de Investigación en Medicina Molecular e Enfermidades Crónicas, Universidade de Santiago de Compostela. Departamento de Bioquímica e Bioloxía Molecular, Universidade de Santiago de Compostela. Departamento de Fisioloxía, Gonzalez-Rellan, Maria J., Parracho, Tamara, Heras, Violeta, Rodriguez, Amaia, Fondevila, Marcos F., Novoa, Eva, Lima, Natalia, Varela-Rey, Marta, Senra, Ana, Chantada-Vazquez, Maria D.P., Ameneiro, Cristina, Bernardo, Ganeko, Fernandez-Ramos, David, Lopitz-Otsoa, Fernando, Bilbao, Jon, Guallar, Diana, Fidalgo, Miguel, Bravo, Susana, Dieguez, Carlos, Martinez-Chantar, Maria L., Millet, Oscar, Mato, Jose M., Schwaninger, Markus, Prevot, Vincent, Crespo, Javier, Frühbeck, Gema, Iruzubieta, Paula, Nogueiras, Ruben, Universidade de Santiago de Compostela. Centro de Investigación en Medicina Molecular e Enfermidades Crónicas, Universidade de Santiago de Compostela. Departamento de Bioquímica e Bioloxía Molecular, Universidade de Santiago de Compostela. Departamento de Fisioloxía, Gonzalez-Rellan, Maria J., Parracho, Tamara, Heras, Violeta, Rodriguez, Amaia, Fondevila, Marcos F., Novoa, Eva, Lima, Natalia, Varela-Rey, Marta, Senra, Ana, Chantada-Vazquez, Maria D.P., Ameneiro, Cristina, Bernardo, Ganeko, Fernandez-Ramos, David, Lopitz-Otsoa, Fernando, Bilbao, Jon, Guallar, Diana, Fidalgo, Miguel, Bravo, Susana, Dieguez, Carlos, Martinez-Chantar, Maria L., Millet, Oscar, Mato, Jose M., Schwaninger, Markus, Prevot, Vincent, Crespo, Javier, Frühbeck, Gema, Iruzubieta, Paula, and Nogueiras, Ruben

Abstract

Objective O-GlcNAcylation is a post-translational modification that directly couples the processes of nutrient sensing, metabolism, and signal transduction, affecting protein function and localization, since the O-linked N-acetylglucosamine moiety comes directly from the metabolism of glucose, lipids, and amino acids. The addition and removal of O-GlcNAc of target proteins are mediated by two highly conserved enzymes: O-linked N-acetylglucosamine (O-GlcNAc) transferase (OGT) and O-GlcNAcase (OGA), respectively. Deregulation of O-GlcNAcylation has been reported to be associated with various human diseases such as cancer, diabetes, and cardiovascular diseases. The contribution of deregulated O-GlcNAcylation to the progression and pathogenesis of NAFLD remains intriguing, and a better understanding of its roles in this pathophysiological context is required to uncover novel avenues for therapeutic intervention. By using a translational approach, our aim is to describe the role of OGT and O-GlcNAcylation in the pathogenesis of NAFLD. Methods We used primary mouse hepatocytes, human hepatic cell lines and in vivo mouse models of steatohepatitis to manipulate O-GlcNAc transferase (OGT). We also studied OGT and O-GlcNAcylation in liver samples from different cohorts of people with NAFLD. Results O-GlcNAcylation was upregulated in the liver of people and animal models with steatohepatitis. Downregulation of OGT in NAFLD-hepatocytes improved diet-induced liver injury in both in vivo and in vitro models. Proteomics studies revealed that mitochondrial proteins were hyper-O-GlcNAcylated in the liver of mice with steatohepatitis. Inhibition of OGT is able to restore mitochondrial oxidation and decrease hepatic lipid content in in vitro and in vivo models of NAFLD. Conclusions These results demonstrate that deregulated hyper-O-GlcNAcylation favors NAFLD progression by reducing mitochondrial oxidation and promoting hepatic lipid accumulation

Published
2023

45. Integrative Metabolic, Lipidomic and Lipoproteomic Modelling of SARS-CoV-2 Infections in Relation to Clinical Severity and Early Mortality Prediction

Author

Lodge, Samantha, Lawler, Nathan, Gray, Nicola, Masuda, Reika, Nitschke, Philipp, Whiley, Luke, Sze-How Bong, Yeap, Bu B., Girish Dwivedi, Spraul, Manfred, Schaefer, Hartmut, Gil-Redondo, Rubén, Embade, Nieves, Millet, Oscar, Holmes, Elaine, Wist, Julien, and Nicholson, Jeremy K.

Subjects
lipoproteins, NMR spectroscopy, metabolic phenotyping, SARS-CoV-2, COVID-19, plasma IVDr, lipidomics, diagnostic modelling, patient stratification, mortality prediction, metabolomics, mass spectrometry
Abstract

An integrative multi-modal metabolic phenotyping model was developed to assess the systemic plasma sequelae of SARS-CoV-2 (rRT-PCR positive) induced COVID-19 disease in patients with different respiratory severity levels. Plasma samples from 306 unvaccinated COVID-19 patients were collected in 2020 and classified into four levels of severity ranging from mild symptoms to severe ventilated cases. These samples were investigated using a combination of quantitative Nuclear Magnetic Resonance (NMR) spectroscopy and Mass Spectrometry (MS) platforms to give broad lipoprotein, lipidomic and amino acid, tryptophan-kynurenine pathway and biogenic amine pathway coverage. All platforms revealed highly significant differences in metabolite patterns between patients and controls (n=89) that had been collected prior to the COVID-19 pandemic. The total number of significant metabolites increased with severity with 344 out of the 1034 quantitative variables being common to all severity classes. Metabolic signatures showed a continuum of changes across the respiratory severity levels with the most significant and extensive changes being in the most severely affected patients. Even mildly affected respiratory patients showed multiple highly significant abnormal biochemical signatures reflecting serious metabolic deficiencies of the type observed in Post acute COVID -19 syndrome patients. The most severe respiratory patients had a high mortality (56.1%) and we found that we could predict mortality in this patient sub-group with high accuracy in some cases up to 61 days prior to death, based on a separate metabolic model, which highlighted a different set of metabolites to those defining the basic disease. Specifically, hexosylceramides (HCER 16:0, HCER 20:0, HCER 24:1, HCER 26:0, HCER 26:1) were markedly elevated in the non-surviving patient group (Cliff’s delta 0.91-0.95) and two phosphoethanolamines (PE.O 18:0/18:1, Cliff’s delta=-0.98 and PE.P 16:0/18:1, Cliff’s delta=-0.93) were markedly lower in the non-survivors. These results indicate that patient morbidity to mortality trajectories are determined relatively soon after infection, opening the opportunity to select more intensive therapeutic interventions to these “high risk” patients in the early disease stages.&nbsp

Published
2023
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47. NMR-based newborn urine screening for optimized detection of inherited errors of metabolism

Author

Embade, Nieves, Cannet, Claire, Diercks, Tammo, Gil-Redondo, Rubén, Bruzzone, Chiara, Ansó, Sara, Echevarría, Lourdes Román, Ayucar, M. Mercedes Martinez, Collazos, Laura, Lodoso, Blanca, Guerra, Eneritz, Elorriaga, Izaskun Asla, Kortajarena, Miguel Ángel, Legorburu, Alberto Pérez, Fang, Fang, Astigarraga, Itziar, Schäfer, Hartmut, Spraul, Manfred, and Millet, Oscar

Published
2019
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50. MetSCORE: A Molecular Metric to Evaluate the Risk of Metabolic Syndrome Based on Serum NMR Metabolomics

Author

Gil-Redondo, Rubén, primary, Conde, Ricardo, additional, Bruzzone, Chiara, additional, Seco, Marisa, additional, Bizkarguenaga, Maider, additional, González-Valle, Beatriz, additional, de Diego, Angela, additional, Laín, Ana, additional, Habisch, Hansjörg, additional, Haudum, Christoph, additional, Verheyen, Nicolas, additional, Obermayer-Pietsch, Barbara, additional, Margarita, Sara, additional, Pelusi, Serena, additional, Verde, Ignacio, additional, Oliveira, Nádia, additional, Sousa, Adriana, additional, Zabala-Letona, Amaia, additional, Santos-Martin, Aida, additional, Loizaga-Iriarte, Ana, additional, Unda-Urzaiz, Miguel, additional, Kazenwadel, Jasmin, additional, Bereznoy, Georgy, additional, Geisler, Tobias, additional, Gawaz, Meinrad, additional, Cannet, Claire, additional, Schäfer, Hartmut, additional, Diercks, Tammo, additional, Trautwein, Christoph, additional, Carracedo, Arkaitz, additional, Madl, Tobias, additional, Valenti, Luca, additional, Spraul, Manfred, additional, Lu, Shelly C., additional, Embade, Nieves, additional, Mato, José M., additional, and Millet, Oscar, additional

Published
2023
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