Inositol hexaphosphate-induced cellular response in myeloid leukemia cells is mediated by nicotinamide adenine dinucleotide phosphate oxidase activation
Objectives: The objective of this study was to identify the role of reactive oxygen species (ROS) generated by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, in inositol hexaphosphate (IP6)-induced metabolic disruption in human leukemia PLB-985 cells. Methods: PLB-985 and X chromosome...
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Language: | English |
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Fujita Medical Society
2019-11-01
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Series: | Fujita Medical Journal |
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Online Access: | https://www.jstage.jst.go.jp/article/fmj/5/4/5_2018-020/_pdf/-char/en |
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author | Asuka Kato Yuki Hirakawa Wakako Hiraoka |
author_facet | Asuka Kato Yuki Hirakawa Wakako Hiraoka |
author_sort | Asuka Kato |
collection | DOAJ |
description | Objectives: The objective of this study was to identify the role of reactive oxygen species (ROS) generated by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, in inositol hexaphosphate (IP6)-induced metabolic disruption in human leukemia PLB-985 cells. Methods: PLB-985 and X chromosome linked gp91-phox gene knockout (X-CGD) cells were treated with 5, 10, or 20 mM IP6 for 24 to 72 h. Cell growth was assayed using a highly water-soluble tetrazolium salt. The rate of apoptotic and necrotic cell death was determined with an Annexin V-fluorescein isothiocyanate/propidium iodide kit. The expression of CD11b as a marker of monocytic property and of LC3 as an autophagy marker was tested, using flow cytometry combined with fluorescent antibodies. Results: Treatment with 5 and 10 mM IP6 for 24 h was found to suppress the growth of both cell lines, though the effect was more dramatic in PLB-985 cells. After 6-h treatment with 20 mM IP6, the necrosis rate of PLB-985 cells was significantly greater than that of X-CGD cells. Further, after 72-h treatment with 10 mM IP6, CD11b expression was observed in PLB-985 cells but inhibited in X-CGD cells. Autophagy monitoring after 6-h treatment with 10 mM IP6 revealed that LC3 expression was suppressed in PLB-985 cells, whereas it was somewhat increased in X-CGD cells. Conclusions: Our results suggest that NADPH oxidase activation mediates IP6-induced metabolic disruption associated with necrosis, differentiation, cell growth, and autophagy in PLB-985 cells. |
first_indexed | 2024-12-12T10:39:27Z |
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id | doaj.art-8bf0002ad6de479c9161d4fb6f363b64 |
institution | Directory Open Access Journal |
issn | 2189-7247 2189-7255 |
language | English |
last_indexed | 2024-12-12T10:39:27Z |
publishDate | 2019-11-01 |
publisher | Fujita Medical Society |
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series | Fujita Medical Journal |
spelling | doaj.art-8bf0002ad6de479c9161d4fb6f363b642022-12-22T00:27:06ZengFujita Medical SocietyFujita Medical Journal2189-72472189-72552019-11-01549810310.20407/fmj.2018-020Inositol hexaphosphate-induced cellular response in myeloid leukemia cells is mediated by nicotinamide adenine dinucleotide phosphate oxidase activationAsuka KatoYuki HirakawaWakako HiraokaObjectives: The objective of this study was to identify the role of reactive oxygen species (ROS) generated by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, in inositol hexaphosphate (IP6)-induced metabolic disruption in human leukemia PLB-985 cells. Methods: PLB-985 and X chromosome linked gp91-phox gene knockout (X-CGD) cells were treated with 5, 10, or 20 mM IP6 for 24 to 72 h. Cell growth was assayed using a highly water-soluble tetrazolium salt. The rate of apoptotic and necrotic cell death was determined with an Annexin V-fluorescein isothiocyanate/propidium iodide kit. The expression of CD11b as a marker of monocytic property and of LC3 as an autophagy marker was tested, using flow cytometry combined with fluorescent antibodies. Results: Treatment with 5 and 10 mM IP6 for 24 h was found to suppress the growth of both cell lines, though the effect was more dramatic in PLB-985 cells. After 6-h treatment with 20 mM IP6, the necrosis rate of PLB-985 cells was significantly greater than that of X-CGD cells. Further, after 72-h treatment with 10 mM IP6, CD11b expression was observed in PLB-985 cells but inhibited in X-CGD cells. Autophagy monitoring after 6-h treatment with 10 mM IP6 revealed that LC3 expression was suppressed in PLB-985 cells, whereas it was somewhat increased in X-CGD cells. Conclusions: Our results suggest that NADPH oxidase activation mediates IP6-induced metabolic disruption associated with necrosis, differentiation, cell growth, and autophagy in PLB-985 cells.https://www.jstage.jst.go.jp/article/fmj/5/4/5_2018-020/_pdf/-char/eninositol hexaphosphatereactive oxygen speciesnadph oxidasex-cgd cellsplb-985 cells |
spellingShingle | Asuka Kato Yuki Hirakawa Wakako Hiraoka Inositol hexaphosphate-induced cellular response in myeloid leukemia cells is mediated by nicotinamide adenine dinucleotide phosphate oxidase activation Fujita Medical Journal inositol hexaphosphate reactive oxygen species nadph oxidase x-cgd cells plb-985 cells |
title | Inositol hexaphosphate-induced cellular response in myeloid leukemia cells is mediated by nicotinamide adenine dinucleotide phosphate oxidase activation |
title_full | Inositol hexaphosphate-induced cellular response in myeloid leukemia cells is mediated by nicotinamide adenine dinucleotide phosphate oxidase activation |
title_fullStr | Inositol hexaphosphate-induced cellular response in myeloid leukemia cells is mediated by nicotinamide adenine dinucleotide phosphate oxidase activation |
title_full_unstemmed | Inositol hexaphosphate-induced cellular response in myeloid leukemia cells is mediated by nicotinamide adenine dinucleotide phosphate oxidase activation |
title_short | Inositol hexaphosphate-induced cellular response in myeloid leukemia cells is mediated by nicotinamide adenine dinucleotide phosphate oxidase activation |
title_sort | inositol hexaphosphate induced cellular response in myeloid leukemia cells is mediated by nicotinamide adenine dinucleotide phosphate oxidase activation |
topic | inositol hexaphosphate reactive oxygen species nadph oxidase x-cgd cells plb-985 cells |
url | https://www.jstage.jst.go.jp/article/fmj/5/4/5_2018-020/_pdf/-char/en |
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