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Perit Dial Int 29(1): 44-51
2009
© 2009 International Society for Peritoneal Dialysis
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Bench

3,4-DIDEOXYGLUCOSONE-3-ENE INDUCES APOPTOSIS IN HUMAN PERITONEAL MESOTHELIAL CELLS

Duk-Hyun Lee1, Soon-Youn Choi2, Hye-Myung Ryu2, Chan-Duck Kim2, Sun-Hee Park2, Ho-Young Chung3, In-San Kim4 and Yong-Lim Kim2

Department of Internal Medicine,1 Daegu Fatima Hospital; Division of Nephrology and Department of Internal Medicine,2 Department of Surgery,3 Department of Biochemistry and Cell and Matrix Research Institute,4 Kyungpook National University School of Medicine, Daegu, Korea

Correspondence to: Y.L. Kim, Division of Nephrology and Department of Internal Medicine, Kyungpook National University Hospital, 50, Samduk-dong 2Ga, Jung-gu, Daegu 700-721, Korea. ylkim{at}knu.ac.kr

{diamondsuit} Objective: Glucose degradation products (GDPs) are formed during heat sterilization and storage of peritoneal dialysis (PD) fluids. 3,4-dideoxyglucosone-3-ene (3,4-DGE) has been identified as the most bioreactive GDP. 3,4-DGE induces apoptosis in leukocytes and renal tubular epithelial cells. Our aim was to evaluate the apoptotic effects of 3,4-DGE on human peritoneal mesothelial cells (HPMCs).

{diamondsuit} Methods: Primary cultured HPMCs were treated with 25 or 50 µmol/L 3,4-DGE. MTT assay was used to determine cell viability. Apoptosis was measured using TUNEL assay and flow cytometry. Expressions of procaspase-3, Bax, and Bcl-2 were estimated by Western blot. Activity of caspase-3 was measured and the effect of the caspase inhibitor zVAD-fmk (Z-Val-Ala-DL-Asp-fluoromethylketone) was evaluated by TUNEL assay.

{diamondsuit} Results: 3,4-DGE treatment accelerated cell death in HPMCs in a dose- and time-dependent manner. Treatment with 3,4-DGE (25 and 50 µmol/L) significantly increased apoptosis compared to control (p < 0.05 and p < 0.01 respectively) by TUNEL assay. Flow cytometry showed treatment with 50 µmol/L 3,4-DGE significantly increased apoptosis compared to control (p < 0.05). Decreased expression of procaspase-3 and increased activity of caspase-3 were observed in the presence of 50 µmol/L 3,4-DGE compared to control and 25 µmol/L 3,4-DGE (p < 0.05). 3,4-DGE-induced HPMC apoptosis was decreased after pretreatment with the pan-caspase inhibitor zVAD-fmk in the 50 µmol/L 3,4-DGE-treated group (p < 0.001). The ratio of Bcl-2 to Bax expression was decreased in the 25 µmol/L and the 50 µmol/L 3,4-DGE-treated groups compared to control (p < 0.05).

{diamondsuit} Conclusions: 3,4-DGE promotes apoptosis in HPMCs by a caspase-related mechanism.

KEY WORDS: 3,4-DGE; peritoneal mesothelial cells; apoptosis; caspase.

Received 23 July 2007; accepted 5 May 2008.






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