Very long chain fatty acid beta-oxidation in astrocytes: contribution of the ABCD1-dependent and -independent pathways
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- Morita Masashi
- Department of Biological Chemistry, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama
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- Shinbo Saori
- Department of Biological Chemistry, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama
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- Asahi Akiko
- Department of Biological Chemistry, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama
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- Imanaka Tsuneo
- Department of Biological Chemistry, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama
書誌事項
- タイトル別名
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- Very Long Chain Fatty Acid β-Oxidation in Astrocytes: Contribution of the ABCD1-Dependent and -Independent Pathways
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抄録
Very long chain fatty acid (VLCFA) metabolism in astrocytes is important for the maintenance of myelin structure in central nervous system. To analyze the contribution of the ABCD1-dependent and -independent pathways to VLCFA metabolism in astrocytes, we prepared human glioblastoma U87 cells with a silencing of ABCD1 and primary astrocytes from abcd1-deficient mice, and measured fatty acid β-oxidation in the presence or absence of a potent inhibitor of carnitine palmitoyltransferase I, 2-[5-(4-chlorophenyl)pentyl]oxirane-2-carboxylate (POCA). In U87 cells, C24:0 β-oxidation was decreased to ca. 70% of the control in the presence of POCA, and the activity was further decreased to ca. 20% by the silencing of ABCD1. In mouse primary astrocytes, C24:0 β-oxidation was also decreased to ca. 70% of the control in the presence of POCA. The C24:0 β-oxidation in Abcd1-deficient primary astrocytes was ca. 60% of the wild-type cells and the activity was further decreased to ca. 25% in the presence of POCA. Compared to human skin fibroblasts, in which VLCFA β-oxidation is not significantly inhibited by POCA, approximately one-third of the overall VLCFA β-oxidation was inhibited in both types of astrocytic cells. These results suggest that VLCFA is indeed β-oxidized in ABCD1-dependent pathway, but the ABCD1-independent peroxisomal and mitochondrial β-oxidation pathways significantly contribute to VLCFA β-oxidation in astrocytic cells.
収録刊行物
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- Ｂｉｏｌｏｇｉｃａｌ ＆ Ｐｈａｒｍａｃｅｕｔｉｃａｌ Ｂｕｌｌｅｔｉｎ
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Ｂｉｏｌｏｇｉｃａｌ ＆ Ｐｈａｒｍａｃｅｕｔｉｃａｌ Ｂｕｌｌｅｔｉｎ 35 (11), 1972-1979, 2012
公益社団法人 日本薬学会
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詳細情報 詳細情報について
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- CRID
- 1390001204633462784
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- NII論文ID
- 130001872256
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- NII書誌ID
- AA10885497
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- COI
- 1:STN:280:DC%2BC3s7gs1Wqsg%3D%3D
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- ISSN
- 13475215
- 09186158
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- NDL書誌ID
- 024032902
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- PubMed
- 23123468
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
- KAKEN
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- 抄録ライセンスフラグ
- 使用不可