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- 倉田 朋
- 名古屋市立大・院薬・細胞分子薬効解析学
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- 鈴木 良明
- 名古屋市立大・院薬・細胞分子薬効解析学
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- 楯野 真也
- 名古屋市立大・院薬・細胞分子薬効解析学
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- 味八木 茂
- 広島大・院医・整形外科学
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- Elva Bernotiene
- Department of Regenerative Medicine・Innovative Medicine Center
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- Wayne Giles
- Department of Physiology & Pharmacology・Cumming School of Medicine・University of Calgary
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- 山村 寿男
- 名古屋市立大・院薬・細胞分子薬効解析学
書誌事項
- タイトル別名
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- Role of Kv1.6 channel in chondrocytes in osteoarthritis
抄録
<p>Osteoarthritis (OA) is a chronic inflammatory disease characterized by a decrease in cartilage matrix, disorders of joint movement, and severe pain. Previous studies have suggested that an increase in intracellular Ca2+ concentration ([Ca2+]i) in chondrocytes is associated with OA progression. However, the mechanism underlying this increased [Ca2+]i is unknown. In the present study, we aimed to elucidate this mechanism and its roles in OA progression. Primary chondrocytes were isolated from C57BL/6 mice, and treated with interleukin (IL)-1β, a major cytokine secreted into synovial fluid during OA. In IL-1β-treated chondrocytes, resting membrane potential was depolarized, and resting [Ca2+]i was increased due to the downregulation of voltage-gated K+ channel, Kv1.6. This downregulation of Kv1.6 was also detected in chondrocytes from OA model mice and OA patients. IL-1β induced depolarization of mitochondrial membrane potential (ΔΨm) and cell death. In contrast, overexpression of Kv1.6 in chondrocytes using adenovirus reduced resting [Ca2+]i, increased ΔΨm, and inhibited cell death. In summary, IL-1β downregulates Kv1.6 and increases resting [Ca2+]i, resulting in mitochondrial Ca2+ overload and subsequent cell death. Our findings may contribute to the understanding of OA pathogenesis and the development of new treatments for OA.</p>
収録刊行物
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- 日本薬理学会年会要旨集
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日本薬理学会年会要旨集 97 (0), 2-B-SS12-2-, 2023
公益社団法人 日本薬理学会
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詳細情報 詳細情報について
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- CRID
- 1390017267762270208
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- ISSN
- 24354953
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- 本文言語コード
- ja
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- データソース種別
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- JaLC
- Crossref
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- 抄録ライセンスフラグ
- 使用不可