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
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