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KMID : 0923620140140050241
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Immune Network
2014 Volume.14 No. 5 p.241 ~ p.248
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5-aminoimidazole-4-carboxamide Riboside Induces Apoptosis Through AMP-activated Protein Kinase-independent and NADPH Oxidase-dependent Pathways
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Wi Sae-Mi
Lee Ki-Young
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Abstract
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It is debatable whether AMP-activated protein kinase (AMPK) activation is involved in anti-apoptotic or pro-apop-totic signaling. AICAR treatment increases AMPK-α1 phos-phorylation, decreases intracellular reactive oxygen species (ROS) levels, and significantly increases Annexin V-positive cells, DNA laddering, and caspase activity in human myeloid cell. AMPK activation is therefore implicated in apoptosis. However, AMPK-α1-knockdown THP-1 cells are more sensi-tive to apoptosis than control THP-1 cells are, suggesting that the apoptosis is AMPK-independent. Low doses of AICAR induce cell proliferation, whereas high doses of AICAR suppress cell proliferation. Moreover, these effects are significantly correlated with the downregulation of intra-cellular ROS, strongly suggesting that AICAR-induced apop-tosis is critically associated with the inhibition of NADPH oxi-dase by AICAR. Collectively, our results demonstrate that in AICAR-induced apoptosis, intracellular ROS levels are far more relevant than AMPK activation.
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KEYWORD
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5-aminoimidazole-4-carboxamide (AICA) ribo-side, AMP-activated protein kinase, Apoptosis, NADPH oxi-dase, Reactive oxygen species, Lymphoid cells
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