EAE-induced upregulation of mitochondrial MnSOD is associated with increases of mitochondrial SGK1 and Tom20 protein in the mouse kidney cortex
Autor: | Xiaoming Zhou, Sharanpreet Hira, Balamuguran Packialakshmi |
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Rok vydání: | 2019 |
Předmět: |
0301 basic medicine
Male Encephalomyelitis Autoimmune Experimental Kidney Cortex Physiology animal diseases Protein subunit Renal cortex Receptors Cell Surface Mitochondrion Protein Serine-Threonine Kinases Cell Line Immediate-Early Proteins Mitochondrial Proteins 03 medical and health sciences Mice 0302 clinical medicine Downregulation and upregulation Mitochondrial Precursor Protein Import Complex Proteins medicine Animals Humans chemistry.chemical_classification Reactive oxygen species urogenital system Kinase Chemistry Superoxide Dismutase fungi Experimental autoimmune encephalomyelitis HEK 293 cells Membrane Transport Proteins medicine.disease Catalase Cell biology Mitochondria Up-Regulation Mice Inbred C57BL enzymes and coenzymes (carbohydrates) 030104 developmental biology medicine.anatomical_structure HEK293 Cells Reactive Oxygen Species 030217 neurology & neurosurgery |
Zdroj: | The journal of physiological sciences : JPS. 69(5) |
ISSN: | 1880-6562 |
Popis: | Our previous demonstration that severe experimental autoimmune encephalomyelitis (EAE) increases MnSOD protein abundance in the mouse kidney cortex led this study to elucidate the underlying mechanism with monensin-treated HEK293 cells as a model. Severe EAE increases mitochondrial protein abundance of SGK1 kinase and Tom20, a critical subunit of mitochondrial translocase in the renal cortex. In HEK293 cells, catalase inhibits monensin-induced increases of mitochondrial SGK1 and Tom20 protein levels. Further, GSK650394, a specific inhibitor of SGK1 reduces monensin-induced increase of mitochondrial protein abundance of Tom20 and MnSOD. Finally, RNAi of Tom20 reduces the effect of monensin on MnSOD. MnSOD and Tom20 physically associate with each other. In conclusion, in HEK293 cells, mitochondrial reactive oxygen species increase protein abundance of mitochondrial SGK1, which leads to a rise of mitochondrial Tom20, resulting in importing MnSOD protein into the mitochondria. This could be a mechanism by which severe EAE up-regulates mitochondrial MnSOD in the kidney cortex. |
Databáze: | OpenAIRE |
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