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KMID : 0848120100350020061
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International Journal of Oral Biology
2010 Volume.35 No. 2 p.61 ~ p.67
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Selenoprotein S Suppression Enhances the Late Stage Differentiation of Proerythrocytes Via SIRT1
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Yang Hee-Young
Chung Kyoung-Jin
Park Hyang-Rim
Han Seong-Jeong
Lee Seung-Rock
Chay Kee-Oh
Kim Ick-Young
Park Byung-Ju
Lee Tae-Hoon
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Abstract
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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 over-expressing SelS wild-type (WT) or one of two SelS point mutants, or . We found that in the K562 cells treated with 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 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 (12 mM), but not in those expressing a SelS mutant. After four days of Ara-C treatment, SelS-WT-expressing cells showed elevated transcription of -globin, -globin, -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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KEYWORD
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SelS, SIRT1, erythrocyte differentiation, FoxO3
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