{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Barahona I"],"funding":["Fundación Ramón Areces","Comunidad de Madrid","Ministry of Economy and Competitiveness | Instituto de Salud Carlos III","Ministry of Economy and Competitiveness | Agencia Estatal de Investigación"],"pagination":["2362-2380"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9751306"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["29(12)"],"pubmed_abstract":["Activation of oval cells (OCs) has been related to hepatocyte injury during chronic liver diseases including non-alcoholic fatty liver disease (NAFLD). However, OCs plasticity can be affected under pathological environments. We previously found protection against hepatocyte cell death by inhibiting protein tyrosine phosphatase 1B (PTP1B). Herein, we investigated the molecular and cellular processes involved in the lipotoxic susceptibility in OCs expressing or not PTP1B. Palmitic acid (PA) induced apoptotic cell death in wild-type (Ptpn1<sup>+/+</sup>) OCs in parallel to oxidative stress and impaired autophagy. This lipotoxic effect was attenuated in OCs lacking Ptpn1 that showed upregulated antioxidant defences, increased unfolded protein response (UPR) signaling, higher endoplasmic reticu"],"journal":["Cell death and differentiation"],"pubmed_title":["Ptpn1 deletion protects oval cells against lipoapoptosis by favoring lipid droplet formation and dynamics."],"pmcid":["PMC9751306"],"funding_grant_id":["PID2019-106982RB-I00","RTI2018-094052-B-100","DEM21 PI01/2021","PID2019-105989RB-I00","CIBERDEM","CB06/03/0001","CB12/03/30002","S2017/BMD-3684","SAF2017-83813-C3-1-R"],"pubmed_authors":["Grillo-Risco R","Moreno-Aliaga MJ","Balsinde J","LaIglesia LM","Garcia-Garcia F","Soler-Vazquez MC","Serra D","Pereira L","Rada P","Barahona I","Valverde AM","Herrero L","Valdecantos MP","Calero-Perez S","Gonzalez-Rodriguez A","Garcia-Monzon C"],"additional_accession":[]},"is_claimable":false,"name":"Ptpn1 deletion protects oval cells against lipoapoptosis by favoring lipid droplet formation and dynamics.","description":"Activation of oval cells (OCs) has been related to hepatocyte injury during chronic liver diseases including non-alcoholic fatty liver disease (NAFLD). However, OCs plasticity can be affected under pathological environments. We previously found protection against hepatocyte cell death by inhibiting protein tyrosine phosphatase 1B (PTP1B). Herein, we investigated the molecular and cellular processes involved in the lipotoxic susceptibility in OCs expressing or not PTP1B. Palmitic acid (PA) induced apoptotic cell death in wild-type (Ptpn1<sup>+/+</sup>) OCs in parallel to oxidative stress and impaired autophagy. This lipotoxic effect was attenuated in OCs lacking Ptpn1 that showed upregulated antioxidant defences, increased unfolded protein response (UPR) signaling, higher endoplasmic reticu","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Dec","modification":"2026-07-14T18:38:20.398Z","creation":"2024-12-04T13:25:08.561Z"},"accession":"S-EPMC9751306","cross_references":{"pubmed":["35681014"],"doi":["10.1038/s41418-022-01023-x"]}}