Int J Oral Biol.
2010 Jun;35(2):61-67.
Selenoprotein S Suppression Enhances the Late Stage Differentiation of Proerythrocytes Via SIRT1
- Affiliations
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- 1Department of Oral Biochemistry, Dental Science Research Institute, The 2 Stage of Brain Korea 21 for Dental School, Chonnam National University, Gwangju 500-757, Korea. thlee83@chonnam.ac.kr
- 2Department of Biochemistry, Center for Aging and Geriatrics, Chonnam National University Medical School, Gwangju 501-190, Korea.
- 3Laboratory of Cellular and Molecular Biochemistry, School of Life Sciences and Biotechnology, Korea University, Seoul 136-701, Korea.
- 4School of Biological Science and Technology, Chonnam National University, Gwangju 500-757, Korea.
Abstract
- Selenoprotein S (SelS) is widely expressed in diverse tissues where it localizes in the plasma membrane and endoplasmic reticulum. We studied the potential function of SelS in erythrocyte differentiation using K562 cells stably overexpressing SelS wild-type (WT) or one of two SelS point mutants, U188S or U188C. We found that in the K562 cells treated with 1 microM Ara-C, SelS gradually declined over five days of treatment. On day 4, intracellular ROS levels were higher in cells expressing SelS-WT than in those expressing a SelS mutant. Moreover, the cell cycle patterns in cells expressing SelS-WT or U188C were similar to the controls. The expression and activation of SIRT1 were also reduced during K562 differentiation. Cells expressing SelS-WT showed elevated SIRT1 expression and activation (phosphorylation), as well as higher levels of FoxO3a expression. SIRT1 activation was diminished slightly in cells expressing SelS-WT after treatment with the ROS scavenger NAC (12mM), but not in those expressing a SelS mutant. After four days of Ara-C treatment, SelS-WT-expressing cells showed elevated transcription of beta-globin, gamma-globin, epsilon-globin, GATA-1 and zfpm-1, whereas cells expressing a SelS mutant did not. These results suggest that the suppression of SelS acts as a trigger for proerythrocyte differentiation via the ROS-mediated downregulation of SIRT1.
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