Difference between revisions of "Fuertes-Agudo 2022 Antioxidants (Basel)"
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|keywords=COX-2, High-resolution respirometry, Ischemia-reperfusion, Liver, Mitochondrial dynamics, Prostaglandins | |keywords=COX-2, High-resolution respirometry, Ischemia-reperfusion, Liver, Mitochondrial dynamics, Prostaglandins | ||
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|mipnetlab=ES Valencia Casado Pinna M | |||
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|area=Respiration | |area=Respiration, Genetic knockout;overexpression | ||
|injuries=Ischemia-reperfusion | |||
|organism=Mouse | |||
|tissues=Liver | |||
|preparations=Isolated mitochondria | |||
|couplingstates=OXPHOS, ET | |||
|pathways=F, N, Gp, CIV, NS, Other combinations, ROX | |||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
|additional=2022-11 | |additional=2022-11 | ||
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Latest revision as of 13:14, 22 November 2022
| Fuertes-Agudo M, Luque-Tévar M, Cucarella C, Brea R, Boscá L, Quintana-Cabrera R, Martín-Sanz P, Casado M (2022) COX-2 expression in hepatocytes improves mitochondrial function after hepatic ischemia-reperfusion injury. |
» Antioxidants (Basel) 11:1724. PMID: 36139798 Open Access
Fuertes-Agudo Marina, Luque-Tevar Maria, Cucarella Carme, Brea Rocio, Bosca Lisardo, Quintana-Cabrera Ruben, Martin-Sanz Paloma, Casado Marta (2022) Antioxidants (Basel)
Abstract: Cyclooxygenase 2 (COX-2) is a key enzyme in prostanoid biosynthesis. The constitutive hepatocyte expression of COX-2 has a protective role in hepatic ischemia-reperfusion (I/R) injury (IRI), decreasing necrosis, reducing reactive oxygen species (ROS) levels, and increasing autophagy and antioxidant and anti-inflammatory response. The physiopathology of IRI directly impacts mitochondrial activity, causing ATP depletion and being the main source of ROS. Using genetically modified mice expressing human COX-2 (h-COX-2 Tg) specifically in hepatocytes, and performing I/R surgery on the liver, we demonstrate that COX-2 expression has a beneficial effect at the mitochondrial level. Mitochondria derived from h-COX-2 Tg mice livers have an increased respiratory rate associated with complex I electron-feeding pathways compared to Wild-type (Wt) littermates, without affecting complex I expression or assembly. Furthermore, Wt-derived mitochondria show a loss of mitochondrial membrane potential (ΔΨm) that correlates to increased proteolysis of fusion-related OPA1 through OMA1 protease activity. All these effects are not observed in h-COX-2 Tg mitochondria, which behave similarly to the Sham condition. These results suggest that COX-2 attenuates IRI at a mitochondrial level, preserving the proteolytic processing of OPA1, in addition to the maintenance of mitochondrial respiration. • Keywords: COX-2, High-resolution respirometry, Ischemia-reperfusion, Liver, Mitochondrial dynamics, Prostaglandins • Bioblast editor: Plangger M • O2k-Network Lab: ES Valencia Casado Pinna M
Labels: MiParea: Respiration, Genetic knockout;overexpression
Stress:Ischemia-reperfusion Organism: Mouse Tissue;cell: Liver Preparation: Isolated mitochondria
Coupling state: OXPHOS, ET
Pathway: F, N, Gp, CIV, NS, Other combinations, ROX
HRR: Oxygraph-2k
2022-11
