Abstract：
: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.
journal_name
Int J Mol Scijournal_title
International journal of molecular sciencesauthors
Mercado-Gómez M,Lopitz-Otsoa F,Azkargorta M,Serrano-Maciá M,Lachiondo-Ortega S,Goikoetxea-Usandizaga N,Rodríguez-Agudo R,Fernández-Ramos D,Bizkarguenaga M,Juan VG,Lectez B,Aloria K,Arizmendi JM,Simon J,Alonso C,Lozano JJ,doi
10.3390/ijms21239043subject
Has Abstractpub_date
2020-11-27 00:00:00issue
23issn
1422-0067pii
ijms21239043journal_volume
21pub_type
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