Effects of Heme Oxygenase-1 Expression in Mycophenolic Acid Induced Apoptosis of Jurkat Cell Lines.
10.4174/jkss.2010.78.6.343
- Author:
Ho Kyun LEE
1
;
Soo Jin CHOI
Author Information
1. Department of Surgery, Chonnam National University Medical School, Chonnam National University, Gwangju, Korea. choisjn@jnu.ac.kr
- Publication Type:Original Article
- Keywords:
Mycophenolic acid;
Jurkat cell;
Heme oxygenase-1
- MeSH:
Apoptosis;
Blotting, Western;
Cell Death;
Cell Survival;
Flow Cytometry;
Heme;
Heme Oxygenase-1;
Humans;
Jurkat Cells;
Mycophenolic Acid;
Permeability;
Propidium;
Reactive Oxygen Species
- From:Journal of the Korean Surgical Society
2010;78(6):343-349
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: This study demonstrates that pharmacologic induction of heme oygenase-1 (HO-1) along with catalytic activation significantly modulated apoptosis of Jurkat cells induced by mycophenolic acid (MPA). METHODS: Cells were cultured with the presence or absence of MPA. Flow cytometric analysis was performed after propidium iodide staining. Western blotting of HO-1, Bcl, and Bax was also performed. Cells were stained 4'-6-Diamidino-2-phenylindole (DAPI) and measured by flow cytometry in the absence or presence of CoPPIX. RESULTS: Treatment of MPA decreased cell viability in a dose- and time-dependent manner. MPA-induced cell death was confirmed as apoptosis characterized by sub G0/G1 phase arrest. Expression of HO-1 assumes a pattern of decline after rising at the initial phase. CoPPIX, HO-1 inducer, significantly inhibited the cisplatin-induced apoptosis. Treatment of MPA resulted in reactive oxygen species (ROS) generation in Jurkat cells. CoPPIX attenuated ROS production in MPA-treated cells. CONCLUSION: This result suggests that the protective mechanism of HO-1 on MPA-induced cytotoxicity is associated with direct inhibition of ROS generation and mitochondrial permeability transition.
