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[Protective effect of over-expression OGCP on HEK293 cells treated by rotenone and mutant Parkin protein]
Chun-Yu Wang1, Bei-Sha Tang, Hai-Nan Zhang
1Department of Neurology, The Second Xiangya Hospital, Central South University, Changsha 410011, China. wcy19@tom.com
Objective:
To study the effect of alpha-ketoglutarate carrier protein (2-oxoglutarate carrier protein, OGCP) and the Parkin protein on HEK293 cell function.
Methods:
The cell apoptosis rate, mitochondrial membrane potential and intracellular reactive oxygen species of HEK293 cells treated with rotenone, OGCP and / or Parkin protein were detected by using flow cytometry methods (FCM).
Results:
(1) Over-expression wild-type Parkin protein and/or OGCP can increase mitochondrial membrane potential of HEK293 cells induced by rotenone, reduce intracellular reactive oxygen species and cell apoptosis rate of HEK293 cells induced by rotenone, while over-expression mutant Parkin (R42P and T240R) protein can decrease the mitochondrial membrane potential of HEK293 cells, especially the HEK293 cells induced by rotenone, but increase intracellular reactive oxygen species and promote apoptosis. (2) In addition, we also found that OGCP can inhibit the increasing of mitochondrial membrane potential and reactive oxygen species and decreasing of cell apoptosis caused by mutant Parkin protein (R42P and T240R).
Conclusion:
(1) Parkin protein and OGCP may be associated with the maintenance of normal function of mitochondria. (2) Over-expression of mutant parkin (R42P and T240R) protein may inhibit mitochondrial function and promote apoptosis. (3) Over-expression OGCP has protective effect on cell toxicity caused by rotenone and mutant parkin protein.
