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Article ; Online: Isolation of the Hepatic Ubiquitome/NEDDylome by Streptavidin Pull-Down Assay in the Biotinylated Ubiquitin (

Serrano-Maciá, Marina / Delgado, Teresa Cardoso / Martínez-Chantar, María Luz

Methods in molecular biology (Clifton, N.J.)

2022 Volume 2602, Page(s) 151–162

Abstract: In the last years, our group and others have uncovered the role of ubiquitin (Ub) and ubiquitin-like proteins such as the neural precursor cell expressed, developmentally downregulated 8 (NEDD8)-mediated modifications in several types of liver disease, ... ...

Abstract	In the last years, our group and others have uncovered the role of ubiquitin (Ub) and ubiquitin-like proteins such as the neural precursor cell expressed, developmentally downregulated 8 (NEDD8)-mediated modifications in several types of liver disease, including nonalcoholic fatty liver disease, liver fibrosis, and hepatocellular carcinoma. For this purpose, we have taken advantage of biotinylated ubiquitin (
MeSH term(s)	Mice ; Animals ; Ubiquitin ; Streptavidin ; Mice, Transgenic ; Ubiquitins/genetics ; Liver Neoplasms ; Mammals
Chemical Substances	Ubiquitin ; Streptavidin (9013-20-1) ; Ubiquitins
Language	English
Publishing date	2022-11-29
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-2859-1_11
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Article: Metallothionein-3 is a multifunctional driver that modulates the development of sorafenib-resistant phenotype in hepatocellular carcinoma cells.

Rodrigo, Miguel Angel Merlos / Michalkova, Hana / Jimenez, Ana Maria Jimenez / Petrlak, Frantisek / Do, Tomas / Sivak, Ladislav / Haddad, Yazan / Kubickova, Petra / de Los Rios, Vivian / Casal, J Ignacio / Serrano-Macia, Marina / Delgado, Teresa C / Boix, Loreto / Bruix, Jordi / Martinez Chantar, Maria L / Adam, Vojtech / Heger, Zbynek

Biomarker research

2024 Volume 12, Issue 1, Page(s) 38

Abstract: Background & aims: Metallothionein-3 (hMT3) is a structurally unique member of the metallothioneins family of low-mass cysteine-rich proteins. hMT3 has poorly characterized functions, and its importance for hepatocellular carcinoma (HCC) cells has not ... ...

Abstract	Background & aims: Metallothionein-3 (hMT3) is a structurally unique member of the metallothioneins family of low-mass cysteine-rich proteins. hMT3 has poorly characterized functions, and its importance for hepatocellular carcinoma (HCC) cells has not yet been elucidated. Therefore, we investigated the molecular mechanisms driven by hMT3 with a special emphasis on susceptibility to sorafenib. Methods: Intrinsically sorafenib-resistant (BCLC-3) and sensitive (Huh7) cells with or without up-regulated hMT3 were examined using cDNA microarray and methods aimed at mitochondrial flux, oxidative status, cell death, and cell cycle. In addition, in ovo/ex ovo chick chorioallantoic membrane (CAM) assays were conducted to determine a role of hMT3 in resistance to sorafenib and associated cancer hallmarks, such as angiogenesis and metastastic spread. Molecular aspects of hMT3-mediated induction of sorafenib-resistant phenotype were delineated using mass-spectrometry-based proteomics. Results: The phenotype of sensitive HCC cells can be remodeled into sorafenib-resistant one via up-regulation of hMT3. hMT3 has a profound effect on mitochondrial respiration, glycolysis, and redox homeostasis. Proteomic analyses revealed a number of hMT3-affected biological pathways, including exocytosis, glycolysis, apoptosis, angiogenesis, and cellular stress, which drive resistance to sorafenib. Conclusions: hMT3 acts as a multifunctional driver capable of inducing sorafenib-resistant phenotype of HCC cells. Our data suggest that hMT3 and related pathways could serve as possible druggable targets to improve therapeutic outcomes in patients with sorafenib-resistant HCC.
Language	English
Publishing date	2024-04-09
Publishing country	England
Document type	Journal Article
ZDB-ID	2699926-2
ISSN	2050-7771
ISSN	2050-7771
DOI	10.1186/s40364-024-00584-y
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Article ; Online: Nutraceutical Properties of Polyphenols against Liver Diseases.

Simón, Jorge / Casado-Andrés, María / Goikoetxea-Usandizaga, Naroa / Serrano-Maciá, Marina / Martínez-Chantar, María Luz

Nutrients

2020 Volume 12, Issue 11

Abstract: Current food tendencies, suboptimal dietary habits and a sedentary lifestyle are spreading metabolic disorders worldwide. Consequently, the prevalence of liver pathologies is increasing, as it is the main metabolic organ in the body. Chronic liver ... ...

Abstract	Current food tendencies, suboptimal dietary habits and a sedentary lifestyle are spreading metabolic disorders worldwide. Consequently, the prevalence of liver pathologies is increasing, as it is the main metabolic organ in the body. Chronic liver diseases, with non-alcoholic fatty liver disease (NAFLD) as the main cause, have an alarming prevalence of around 25% worldwide. Otherwise, the consumption of certain drugs leads to an acute liver failure (ALF), with drug-induced liver injury (DILI) as its main cause, or alcoholic liver disease (ALD). Although programs carried out by authorities are focused on improving dietary habits and lifestyle, the long-term compliance of the patient makes them difficult to follow. Thus, the supplementation with certain substances may represent a more easy-to-follow approach for patients. In this context, the consumption of polyphenol-rich food represents an attractive alternative as these compounds have been characterized to be effective in ameliorating liver pathologies. Despite of their structural diversity, certain similar characteristics allow to classify polyphenols in 5 groups: stilbenes, flavonoids, phenolic acids, lignans and curcuminoids. Herein, we have identified the most relevant compounds in each group and characterized their main sources. By this, authorities should encourage the consumption of polyphenol-rich products, as most of them are available in quotidian life, which might reduce the socioeconomical burden of liver diseases.
MeSH term(s)	Antioxidants/pharmacology ; Diarylheptanoids ; Dietary Supplements ; Flavonoids ; Humans ; Hydroxybenzoates ; Life Style ; Lignans ; Liver Diseases/epidemiology ; Liver Diseases/prevention & control ; Polyphenols/chemistry ; Polyphenols/pharmacology ; Stilbenes
Chemical Substances	Antioxidants ; Diarylheptanoids ; Flavonoids ; Hydroxybenzoates ; Lignans ; Polyphenols ; Stilbenes ; phenolic acid (I3P9R8317T)
Language	English
Publishing date	2020-11-15
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2518386-2
ISSN	2072-6643 ; 2072-6643
ISSN (online)	2072-6643
ISSN	2072-6643
DOI	10.3390/nu12113517
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Article ; Online: Enhanced mitochondrial activity reshapes a gut microbiota profile that delays NASH progression.

Juárez-Fernández, María / Goikoetxea-Usandizaga, Naroa / Porras, David / García-Mediavilla, María Victoria / Bravo, Miren / Serrano-Maciá, Marina / Simón, Jorge / Delgado, Teresa C / Lachiondo-Ortega, Sofía / Martínez-Flórez, Susana / Lorenzo, Óscar / Rincón, Mercedes / Varela-Rey, Marta / Abecia, Leticia / Rodríguez, Héctor / Anguita, Juan / Nistal, Esther / Martínez-Chantar, María Luz / Sánchez-Campos, Sonia

Hepatology (Baltimore, Md.)

2023 Volume 77, Issue 5, Page(s) 1654–1669

Abstract: Background and aims: Recent studies suggest that mitochondrial dysfunction promotes progression to NASH by aggravating the gut-liver status. However, the underlying mechanism remains unclear. Herein, we hypothesized that enhanced mitochondrial activity ... ...

Abstract	Background and aims: Recent studies suggest that mitochondrial dysfunction promotes progression to NASH by aggravating the gut-liver status. However, the underlying mechanism remains unclear. Herein, we hypothesized that enhanced mitochondrial activity might reshape a specific microbiota signature that, when transferred to germ-free (GF) mice, could delay NASH progression. Approach and results: Wild-type and methylation-controlled J protein knockout (MCJ-KO) mice were fed for 6 weeks with either control or a choline-deficient, L-amino acid-defined, high-fat diet (CDA-HFD). One mouse of each group acted as a donor of cecal microbiota to GF mice, who also underwent the CDA-HFD model for 3 weeks. Hepatic injury, intestinal barrier, gut microbiome, and the associated fecal metabolome were then studied. Following 6 weeks of CDA-HFD, the absence of methylation-controlled J protein, an inhibitor of mitochondrial complex I activity, reduced hepatic injury and improved gut-liver axis in an aggressive NASH dietary model. This effect was transferred to GF mice through cecal microbiota transplantation. We suggest that the specific microbiota profile of MCJ-KO, characterized by an increase in the fecal relative abundance of Dorea and Oscillospira genera and a reduction in AF12 , Allboaculum , and [ Ruminococcus ], exerted protective actions through enhancing short-chain fatty acids, nicotinamide adenine dinucleotide (NAD + ) metabolism, and sirtuin activity, subsequently increasing fatty acid oxidation in GF mice. Importantly, we identified Dorea genus as one of the main modulators of this microbiota-dependent protective phenotype. Conclusions: Overall, we provide evidence for the relevance of mitochondria-microbiota interplay during NASH and that targeting it could be a valuable therapeutic approach.
MeSH term(s)	Mice ; Animals ; Non-alcoholic Fatty Liver Disease/metabolism ; Gastrointestinal Microbiome/genetics ; Mice, Inbred C57BL ; Liver/metabolism ; Diet, High-Fat/adverse effects ; Molecular Chaperones/metabolism ; Mitochondrial Proteins/metabolism
Chemical Substances	Mcj protein, mouse ; Molecular Chaperones ; Mitochondrial Proteins
Language	English
Publishing date	2023-04-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	604603-4
ISSN	1527-3350 ; 0270-9139
ISSN (online)	1527-3350
ISSN	0270-9139
DOI	10.1002/hep.32705
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Article ; Online: Corrigendum to "In utero exposure to bisphenol-A disrupts key elements of retinoid system in male mice offspring".

Esteban, Javier / Serrano-Maciá, Marina / Sánchez-Perez, Ismael / Alonso-Magdalena, Paloma / Pellín, María de la Cruz / García-Arévalo, Marta / Nadal, Ángel / Barril, Jose

Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association

2021 Volume 158, Page(s) 112556

Language	English
Publishing date	2021-09-20
Publishing country	England
Document type	Published Erratum
ZDB-ID	782617-5
ISSN	1873-6351 ; 0278-6915
ISSN (online)	1873-6351
ISSN	0278-6915
DOI	10.1016/j.fct.2021.112556
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Article: In utero exposure to bisphenol-A disrupts key elements of retinoid system in male mice offspring

Esteban, Javier / Alonso-Magdalena, Paloma / Barril, Jose / García-Arévalo, Marta / Nadal, Ángel / Pellín, María de la Cruz / Sánchez-Pérez, Ismael / Serrano-Maciá, Marina

Food and chemical toxicology. 2019 Apr., v. 126

2019

Abstract: The retinoid system controls essential cellular processes including mitosis, differentiation and metabolism among others. Although the retinoid-signalling pathway is a potential target for the action of several endocrine disrupting chemicals (EDCs), the ... ...

Abstract	The retinoid system controls essential cellular processes including mitosis, differentiation and metabolism among others. Although the retinoid-signalling pathway is a potential target for the action of several endocrine disrupting chemicals (EDCs), the information about the developmental effects of bisphenol-A (BPA) on the hepatic retinoid system is scarce. Herein, male mice were in utero exposed to BPA following maternal subcutaneous doses of 0, 10 and 100 μg/kg bw/day from gestational day 9–16 and they were sacrificed at post-natal day 30. Retinoid concentrations and gene expression of key elements involved in the retinoid system were determined in liver. BPA increased all-trans-retinoic acid concentration and expression of Adh1, Aox1 and Cyp1a2 (biosynthesis of retinoic acid), while reduced Mrp3 (efflux from hepatocyte to blood), increased Bcrp expression (biliary excretion) and changed the retinoid-dependent signalling system after reducing expression of Rxrβ and increasing that of Fgf21. Furthermore, we found bivariate associations of Rarγ and Rxrγ expressions with all-trans-retinoic acid concentrations and of Fgf21 expression with that of Rarγ. Those findings occurred in animals which showed altered pancreatic function and impaired glucose metabolism during adulthood. The present information should be useful for enhancing testing methods for the identification of EDCs.
Keywords	adulthood ; biosynthesis ; bisphenol A ; blood ; endocrine-disrupting chemicals ; excretion ; glucose ; liver ; males ; maternal exposure ; mice ; mitosis ; progeny ; retinoic acid ; toxicology
Language	English
Dates of publication	2019-04
Size	p. 142-151.
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	782617-5
ISSN	1873-6351 ; 0278-6915
ISSN (online)	1873-6351
ISSN	0278-6915
DOI	10.1016/j.fct.2019.02.023
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Article: Neddylation tunes peripheral blood mononuclear cells immune response in COVID-19 patients.

Cell death discovery

2022 Volume 8, Issue 1, Page(s) 316

Abstract: The COVID-19 pandemic caused by SARS-CoV-2 has reached 5.5 million deaths worldwide, generating a huge impact globally. This highly contagious viral infection produces a severe acute respiratory syndrome that includes cough, mucus, fever and pneumonia. ... ...

Abstract	The COVID-19 pandemic caused by SARS-CoV-2 has reached 5.5 million deaths worldwide, generating a huge impact globally. This highly contagious viral infection produces a severe acute respiratory syndrome that includes cough, mucus, fever and pneumonia. Likewise, many hospitalized patients develop severe pneumonia associated with acute respiratory distress syndrome (ARDS), along an exacerbated and uncontrolled systemic inflammation that in some cases induces a fatal cytokine storm. Although vaccines clearly have had a beneficial effect, there is still a high percentage of unprotected patients that develop the pathology, due to an ineffective immune response. Therefore, a thorough understanding of the modulatory mechanisms that regulate the response to SARS-CoV-2 is crucial to find effective therapeutic alternatives. Previous studies describe the relevance of Neddylation in the activation of the immune system and its implications in viral infection. In this context, the present study postulates Neddylation, a reversible ubiquitin-like post-translational modification of proteins that control their stability, localization and activity, as a key regulator in the immune response against SARS-CoV-2. For the first time, we describe an increase in global neddylation levels in COVID-19 in the serum of patients, which is particularly associated with the early response to infection. In addition, the results showed that overactivation of neddylation controls activation, proliferation, and response of peripheral blood mononuclear cells (PBMCs) isolated from COVID-19 patients. Inhibition of neddylation, and the subsequent avoidance of activated PBMCs, reduces cytokine production, mainly IL-6 and MCP-1 and induce proteome modulation, being a critical mechanism and a potential approach to immunomodulate COVID-19 patients.
Language	English
Publishing date	2022-07-12
Publishing country	United States
Document type	Journal Article
ISSN	2058-7716
ISSN	2058-7716
DOI	10.1038/s41420-022-01115-0
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Article ; Online: Neddylation of phosphoenolpyruvate carboxykinase 1 controls glucose metabolism.

Gonzalez-Rellan, María J / Fernández, Uxía / Parracho, Tamara / Novoa, Eva / Fondevila, Marcos F / da Silva Lima, Natalia / Ramos, Lucía / Rodríguez, Amaia / Serrano-Maciá, Marina / Perez-Mejias, Gonzalo / Chantada-Vazquez, Pilar / Riobello, Cristina / Veyrat-Durebex, Christelle / Tovar, Sulay / Coppari, Roberto / Woodhoo, Ashwin / Schwaninger, Markus / Prevot, Vincent / Delgado, Teresa C /

Lopez, Miguel / Diaz-Quintana, Antonio / Dieguez, Carlos / Guallar, Diana / Frühbeck, Gema / Diaz-Moreno, Irene / Bravo, Susana B / Martinez-Chantar, Maria L / Nogueiras, Ruben

Cell metabolism

2023 Volume 35, Issue 9, Page(s) 1630–1645.e5

Abstract: Neddylation is a post-translational mechanism that adds a ubiquitin-like protein, namely neural precursor cell expressed developmentally downregulated protein 8 (NEDD8). Here, we show that neddylation in mouse liver is modulated by nutrient availability. ...

Abstract	Neddylation is a post-translational mechanism that adds a ubiquitin-like protein, namely neural precursor cell expressed developmentally downregulated protein 8 (NEDD8). Here, we show that neddylation in mouse liver is modulated by nutrient availability. Inhibition of neddylation in mouse liver reduces gluconeogenic capacity and the hyperglycemic actions of counter-regulatory hormones. Furthermore, people with type 2 diabetes display elevated hepatic neddylation levels. Mechanistically, fasting or caloric restriction of mice leads to neddylation of phosphoenolpyruvate carboxykinase 1 (PCK1) at three lysine residues-K278, K342, and K387. We find that mutating the three PCK1 lysines that are neddylated reduces their gluconeogenic activity rate. Molecular dynamics simulations show that neddylation of PCK1 could re-position two loops surrounding the catalytic center into an open configuration, rendering the catalytic center more accessible. Our study reveals that neddylation of PCK1 provides a finely tuned mechanism of controlling glucose metabolism by linking whole nutrient availability to metabolic homeostasis.
MeSH term(s)	Mice ; Animals ; Phosphoenolpyruvate/metabolism ; Diabetes Mellitus, Type 2/metabolism ; Proteins/metabolism ; Liver/metabolism ; Lysine/metabolism ; Glucose/metabolism
Chemical Substances	Phosphoenolpyruvate (73-89-2) ; Proteins ; Lysine (K3Z4F929H6) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2023-08-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2176834-1
ISSN	1932-7420 ; 1550-4131
ISSN (online)	1932-7420
ISSN	1550-4131
DOI	10.1016/j.cmet.2023.07.003
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Article ; Online: The Balance between Mono- and NEDD8-Chains Controlled by NEDP1 upon DNA Damage Is a Regulatory Module of the HSP70 ATPase Activity.

Bailly, Aymeric P / Perrin, Aurelien / Serrano-Macia, Marina / Maghames, Chantal / Leidecker, Orsolya / Trauchessec, Helene / Martinez-Chantar, M L / Gartner, Anton / Xirodimas, Dimitris P

Cell reports

2019 Volume 29, Issue 1, Page(s) 212–224.e8

Abstract: Ubiquitin and ubiquitin-like chains are finely balanced by conjugating and de-conjugating enzymes. Alterations in this balance trigger the response to stress conditions and are often observed in pathologies. How such changes are detected is not well ... ...

Abstract	Ubiquitin and ubiquitin-like chains are finely balanced by conjugating and de-conjugating enzymes. Alterations in this balance trigger the response to stress conditions and are often observed in pathologies. How such changes are detected is not well understood. We identify the HSP70 chaperone as a sensor of changes in the balance between mono- and poly-NEDDylation. Upon DNA damage, the induction of the de-NEDDylating enzyme NEDP1 restricts the formation of NEDD8 chains, mainly through lysines K11/K48. This promotes APAF1 oligomerization and apoptosis induction, a step that requires the HSP70 ATPase activity. HSP70 binds to NEDD8, and, in vitro, the conversion of NEDD8 chains into mono-NEDD8 stimulates HSP70 ATPase activity. This effect is independent of NEDD8 conjugation onto substrates. The study indicates that the NEDD8 cycle is a regulatory module of HSP70 function. These findings may be important in tumorigenesis, as we find decreased NEDP1 levels in hepatocellular carcinoma with concomitant accumulation of NEDD8 conjugates.
MeSH term(s)	Adenosine Triphosphatases/genetics ; Amino Acid Sequence ; Animals ; Carcinogenesis/genetics ; Cell Line, Tumor ; DNA Damage/genetics ; Endopeptidases/genetics ; Female ; HSP70 Heat-Shock Proteins/genetics ; Humans ; Lysine/genetics ; MCF-7 Cells ; Mice ; NEDD8 Protein/genetics ; Ubiquitin/genetics
Chemical Substances	HSP70 Heat-Shock Proteins ; NEDD8 Protein ; NEDD8 protein, human ; Ubiquitin ; Endopeptidases (EC 3.4.-) ; SENP8 protein, human (EC 3.4.22.-) ; Adenosine Triphosphatases (EC 3.6.1.-) ; Lysine (K3Z4F929H6)
Language	English
Publishing date	2019-10-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2019.08.070
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Article ; Online: Ubiquitin-Like Post-Translational Modifications (Ubl-PTMs): Small Peptides with Huge Impact in Liver Fibrosis.

Lachiondo-Ortega, Sofia / Mercado-Gómez, Maria / Serrano-Maciá, Marina / Lopitz-Otsoa, Fernando / Salas-Villalobos, Tanya B / Varela-Rey, Marta / Delgado, Teresa C / Martínez-Chantar, María Luz

Cells

2019 Volume 8, Issue 12

Abstract: Liver fibrosis is characterized by the excessive deposition of extracellular matrix proteins including collagen that occurs in most types of chronic liver disease. Even though our knowledge of the cellular and molecular mechanisms of liver fibrosis has ... ...

Abstract	Liver fibrosis is characterized by the excessive deposition of extracellular matrix proteins including collagen that occurs in most types of chronic liver disease. Even though our knowledge of the cellular and molecular mechanisms of liver fibrosis has deeply improved in the last years, therapeutic approaches for liver fibrosis remain limited. Profiling and characterization of the post-translational modifications (PTMs) of proteins, and more specifically NEDDylation and SUMOylation ubiquitin-like (Ubls) modifications, can provide a better understanding of the liver fibrosis pathology as well as novel and more effective therapeutic approaches. On this basis, in the last years, several studies have described how changes in the intermediates of the Ubl cascades are altered during liver fibrosis and how specific targeting of particular enzymes mediating these ubiquitin-like modifications can improve liver fibrosis, mainly in in vitro models of hepatic stellate cells, the main fibrogenic cell type, and in pre-clinical mouse models of liver fibrosis. The development of novel inhibitors of the Ubl modifications as well as novel strategies to assess the modified proteome can provide new insights into the overall role of Ubl modifications in liver fibrosis.
MeSH term(s)	Animals ; Humans ; Liver Cirrhosis/metabolism ; Nedd4 Ubiquitin Protein Ligases/metabolism ; Small Ubiquitin-Related Modifier Proteins/metabolism ; Ubiquitination
Chemical Substances	Small Ubiquitin-Related Modifier Proteins ; Nedd4 Ubiquitin Protein Ligases (EC 2.3.2.26)
Language	English
Publishing date	2019-12-04
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells8121575
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