Transient Receptor Potential Melastatin 3 Is Functionally Expressed in Oligodendrocyte Precursor Cells and Is Upregulated in Ischemic Demyelinated Lesions : Highlighted Paper selected by Editor-in-Chief

• Ohashi Kana

  Department of Molecular Pharmacology, Graduate School of Pharmaceutical Sciences, Kyoto University

• Shibasaki Koji

  Division of Neurochemistry, Graduate School of Human Health Science, University of Nagasaki

• Nakazawa Hayaki

  Department of Molecular Pharmacology, Graduate School of Pharmaceutical Sciences, Kyoto University

• Kunimasa Ryotaro

  Department of Molecular Pharmacology, Graduate School of Pharmaceutical Sciences, Kyoto University

• Nagayasu Kazuki

  Department of Molecular Pharmacology, Graduate School of Pharmaceutical Sciences, Kyoto University

• Shirakawa Hisashi

  Department of Molecular Pharmacology, Graduate School of Pharmaceutical Sciences, Kyoto University

• Kaneko Shuji

  Department of Molecular Pharmacology, Graduate School of Pharmaceutical Sciences, Kyoto University

書誌事項

タイトル別名

• Transient Receptor Potential Melastatin 3 Is Functionally Expressed in Oligodendrocyte Precursor Cells and Is Upregulated in Ischemic Demyelinated Lesions

抄録

Oligodendrocyte precursor cells (OPCs) are glial cells that differentiate into oligodendrocytes and myelinate axons. The number of OPCs is reportedly increased in brain lesions in some demyelinating diseases and during ischemia; however, these cells also secrete cytokines and elicit both protective and deleterious effects in response to brain injury. The mechanism regulating the behaviors of OPCs in physiological and pathological conditions must be elucidated to control these cells and to treat demyelinating diseases. Here, we focused on transient receptor potential melastatin 3 (TRPM3), a Ca²⁺-permeable channel that is activated by the neurosteroid pregnenolone sulfate (PS) and body temperature. Trpm3⁺/Pdgfra⁺ OPCs were detected in the cerebral cortex (CTX) and corpus callosum (CC) of P4 and adult rats by in situ hybridization. Trpm3 expression was detected in primary cultured rat OPCs and was increased by treatment with tumor necrosis factor α (TNFα). Application of PS (30–100 µM) increased the Ca²⁺ concentration in OPCs and this effect was inhibited by co-treatment with the TRP channel blocker Gd³⁺ (100 µM) or the TRPM3 inhibitor isosakuranetin (10 µM). Stimulation of TRPM3 with PS (50 µM) did not affect the differentiation or migration of OPCs. The number of Trpm3⁺ OPCs was markedly increased in demyelinated lesions in an endothelin-1 (ET-1)-induced ischemic rat model. In conclusion, TRPM3 is functionally expressed in OPCs in vivo and in vitro and is upregulated in inflammatory conditions such as ischemic insults and TNFα treatment, implying that TRPM3 is involved in the regulation of specific behaviors of OPCs in pathological conditions.

収録刊行物

• Ｂｉｏｌｏｇｉｃａｌ　＆　Ｐｈａｒｍａｃｅｕｔｉｃａｌ　Ｂｕｌｌｅｔｉｎ

  Ｂｉｏｌｏｇｉｃａｌ　＆　Ｐｈａｒｍａｃｅｕｔｉｃａｌ　Ｂｕｌｌｅｔｉｎ 44 (2), 181-187, 2021-02-01

  公益社団法人 日本薬学会

キーワード

• oligodendrocyte precursor cell
• ischemia
• Ca²⁺ imaging
• demyelination
• transient receptor potential melastatin 3

詳細情報

• CRID: 1390286981380764160
• NII論文ID: 130007979613
• NII書誌ID: AA10885497
• DOI: 10.1248/bpb.b20-00510
• ISSN: 13475215
• ISSN: 09186158
• NDL書誌ID: 031242390
• PubMed: 33518671
• Web Site: https://ndlsearch.ndl.go.jp/books/R000000004-I031242390
• Web Site: https://www.jstage.jst.go.jp/article/bpb/44/2/44_b20-00510/_pdf
• Web Site: https://search.jamas.or.jp/link/ui/2022017604
• 本文言語コード: en
• データソース種別:
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  • Crossref
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