Aloria, K. (Kerman)

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2018 - 20202

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    Multi-Omics Integration Highlights the Role of Ubiquitination in CCl4-Induced Liver Fibrosis
    (2020) Banales, J.M. (Jesús M.); Simon, J. (Jorge); Elortza, F. (Felix); Gutiérrez-de-Juan, V. (Virginia); Lozano, J.J. (Juan J.); Mercado-Gómez, M. (Maria); Azkargorta, M. (Mikel); Goikoetxea-Usandizaga, N. (Naroa); Avila, M.A. (Matías Antonio); Alonso, C. (Cristina); Arizmendi, J.M. (Jesús M.); Beraza, N. (Naiara); Lachiondo-Ortega, S. (Sofia); Rodríguez-Agudo, R. (Rubén); Delgado, T.C. (Teresa C.); Aloria, K. (Kerman); Lopitz-Otsoa, F. (Fernando); Fernández-Ramos, D. (David); Mayor, U. (Ugo); Barrio, R. (Rosa); Bizkarguenaga, M. (Maider); Mato, J.M. (José María); Sutherland, J.D. (James D.); Martinez-Chantar, M.L. (María Luz); Marin, J.J.G (Jose J.G.); Lectez, B. (Benoît); Serrano-Macia, M. (Marina)
    Liver fibrosis is the excessive accumulation of extracellular matrix proteins that occurs in chronic liver disease. Ubiquitination is a post-translational modification that is crucial for a plethora of physiological processes. Even though the ubiquitin system has been implicated in several human diseases, the role of ubiquitination in liver fibrosis remains poorly understood. Here, multi-omics approaches were used to address this. Untargeted metabolomics showed that carbon tetrachloride (CCl4)-induced liver fibrosis promotes changes in the hepatic metabolome, specifically in glycerophospholipids and sphingolipids. Gene ontology analysis of public deposited gene array-based data and validation in our mouse model showed that the biological process “protein polyubiquitination” is enriched after CCl4-induced liver fibrosis. Finally, by using transgenic mice expressing biotinylated ubiquitin (bioUb mice), the ubiquitinated proteome was isolated and characterized by mass spectrometry in order to unravel the hepatic ubiquitinated proteome fingerprint in CCl4-induced liver fibrosis. Under these conditions, ubiquitination appears to be involved in the regulation of cell death and survival, cell function, lipid metabolism, and DNA repair. Finally, ubiquitination of proliferating cell nuclear antigen (PCNA) is induced during CCl4-induced liver fibrosis and associated with the DNA damage response (DDR). Overall, hepatic ubiquitome profiling can highlight new therapeutic targets for the clinical management of liver fibrosis.
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    In-depth proteomic characterization of classical and non-classical monocyte subsets
    (MDPI AG, 2018) García, F. (Fernando); Zarzuela, E. (Eduardo); Paradela, A. (Alberto); Corrales, F.J. (Fernando José); Fuentes, M. (Manuel); Garin-Muga, A. (Alba); Díez, P. (Paula); Orfao, A. (Alberto); Sanchez-del-Pino, M.M. (Manuel M.); Garcia-Montero, A. (A.); Beaskoetxea, J. (Javier); Cantero, L. (Laura); Arizmendi, J.M. (Jesús M.); Dégano, R.M. (Rosa M.); Navajas, R. (Rosana); Aloria, K. (Kerman); Muñoz, J. (Javier); Segura, V. (Víctor); Valero, M.L. (María L.)
    Monocytes are bone marrow-derived leukocytes that are part of the innate immune system. Monocytes are divided into three subsets: classical, intermediate and non-classical, which can be differentiated by their expression of some surface antigens, mainly CD14 and CD16. These cells are key players in the inflammation process underlying the mechanism of many diseases. Thus, the molecular characterization of these cells may provide very useful information for understanding their biology in health and disease. We performed a multicentric proteomic study with pure classical and non-classical populations derived from 12 healthy donors. The robust workflow used provided reproducible results among the five participating laboratories. Over 5000 proteins were identified, and about half of them were quantified using a spectral counting approach. The results represent the protein abundance catalogue of pure classical and enriched non-classical blood peripheral monocytes, and could serve as a reference dataset of the healthy population. The functional analysis of the differences between cell subsets supports the consensus roles assigned to human monocytes.