No Evidence for a Basal, Retinoic, or Superoxide-induced Uncoupling Activity of the Uncoupling Protein 2 Present in Spleen or Lung Mitochondria
| Autor: | Maria del Mar Gonzalez-Barroso, Frédéric Bouillaud, Marie-Clotilde Alves-Guerra, Daniel Ricquier, Marc Goubern, Elodie Couplan |
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| Přispěvatelé: | Ceremod CNRS UPR9078, 9 rue Jules Hetzel, Meudon 92190, France. |
| Jazyk: | angličtina |
| Rok vydání: | 2002 |
| Předmět: |
[SDV]Life Sciences [q-bio]
Retinoic acid Spleen Stimulation Tretinoin Mitochondrion Biology Kidney Biochemistry Ion Channels Membrane Potentials Mitochondrial Proteins 03 medical and health sciences chemistry.chemical_compound Mice 0302 clinical medicine Oxygen Consumption Superoxides Proton transport medicine Uncoupling protein Animals Rhodamine 123 Uncoupling Protein 2 RNA Messenger Inner mitochondrial membrane Molecular Biology Lung ComputingMilieux_MISCELLANEOUS 030304 developmental biology Mice Knockout 0303 health sciences Superoxide Membrane Transport Proteins Proteins Cell Biology Flow Cytometry Molecular biology Mitochondria medicine.anatomical_structure Phenotype chemistry 030217 neurology & neurosurgery |
| Zdroj: | Journal of Biological Chemistry Journal of Biological Chemistry, American Society for Biochemistry and Molecular Biology, 2002, 277 (29), pp.26268-26275. ⟨10.1074/jbc.M202535200⟩ |
| ISSN: | 0021-9258 1083-351X |
| DOI: | 10.1074/jbc.M202535200⟩ |
| Popis: | The phenotypes observed in mice whose uncoupling protein (Ucp2) gene had been invalidated by homologous recombination (Ucp2(-/-) mice) are consistent with an increase in mitochondrial membrane potential in macrophages and pancreatic beta cells. This could support an uncoupling (proton transport) activity of UCP2 in the inner mitochondrial membrane in vivo. We used mitochondria from lung or spleen, the two organs expressing the highest level of UCP2, to compare the proton leak of the mitochondrial inner membrane of wild-type and Ucp2(-/-) mice. No difference was observed under basal conditions. Previous reports have concluded that retinoic acid and superoxide activate proton transport by UCP2. Spleen mitochondria showed a higher sensitivity to retinoic acid than liver mitochondria, but this was not caused by UCP2. In contrast with a previous report, superoxide failed to increase the proton leak rate in kidney mitochondria, where no UCP2 expression was detected, and also in spleen mitochondria, which does not support stimulation of UCP2 uncoupling activity by superoxide. Finally, no increase in the ATP/ADP ratio was observed in spleen or lung of Ucp2(-/-) mice. Therefore, no evidence could be gathered for the uncoupling activity of the UCP2 present in spleen or lung mitochondria. Although this may be explained by difficulties with isolated mitochondria, it may also indicate that UCP2 has another physiological significance in spleen and lung. |
| Databáze: | OpenAIRE |
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