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However, the effects of SAA/LPC on human coronary artery smooth muscle cells (hCASMCs) have not been investigated. Therefore, I examined the effects of SAA/LPC on Ca2+/Mg2+ mobilization and its underlying mechanisms in hCASMCs. Methods: Intracellular Ca2+/Mg2+ concentration ([Ca2+]i/[Mg2+]i) was measured with fura-2 AM/mag-fura-2 AM. The conventional/real-time quantitative RT-PCR, Western blot and immunocytochemistry were applied. Small interfering RNA (siRNA) for TRPC4 was used to knock down TRPC4. Result: SAA/LPC increased [Ca2+]i by Ca2+ entry. The SAA-induced Ca2+ entry was inhibited by Gd3+, SKF96365 and 2-aminoethoxydiphenyl borate (2-APB), but not nifedipine. The LPC-induced Ca2+ entry was blocked by Gd3+, but not nifedipine, SKF96365 and 2-APB. U73122 and PTX prevented the activation of SAA-, but not LPC-induced Ca2+ influx. LPC, but not SAA, increased [Mg2+]i. 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Effects of Serum Amyloid A and Lysophosphatidylcholine on Human Coronary Artery Smooth Muscle Cells : Roles of Transient Receptor Potential Channels
https://doi.org/10.15083/00004069
https://doi.org/10.15083/000040694fdf3547-4f9b-4623-856d-301bf36e94ab
名前 / ファイル | ライセンス | アクション |
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h22_tanaka.pdf (1.4 MB)
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Item type | 学位論文 / Thesis or Dissertation(1) | |||||
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公開日 | 2012-11-08 | |||||
タイトル | ||||||
タイトル | Effects of Serum Amyloid A and Lysophosphatidylcholine on Human Coronary Artery Smooth Muscle Cells : Roles of Transient Receptor Potential Channels | |||||
言語 | ||||||
言語 | eng | |||||
資源タイプ | ||||||
資源 | http://purl.org/coar/resource_type/c_46ec | |||||
タイプ | thesis | |||||
ID登録 | ||||||
ID登録 | 10.15083/00004069 | |||||
ID登録タイプ | JaLC | |||||
その他のタイトル | ||||||
その他のタイトル | ヒト冠動脈平滑筋におけるSerum Amyloid A及びLysophosphatidylcholineの生理作用 : TRPチャネルの役割 | |||||
著者 |
Tanaka, Tomofumi
× Tanaka, Tomofumi |
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著者別名 | ||||||
識別子 | 9400 | |||||
識別子Scheme | WEKO | |||||
姓名 | 田中, 悌史 | |||||
著者所属 | ||||||
著者所属 | 東京大学大学院医学系研究科内科学専攻 | |||||
Abstract | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Background: Serum amyloid A (SAA) and lysophosphatidylcholine (LPC) contribute to physiological processes of atherosclerosis and cardiovascular disease. However, the effects of SAA/LPC on human coronary artery smooth muscle cells (hCASMCs) have not been investigated. Therefore, I examined the effects of SAA/LPC on Ca2+/Mg2+ mobilization and its underlying mechanisms in hCASMCs. Methods: Intracellular Ca2+/Mg2+ concentration ([Ca2+]i/[Mg2+]i) was measured with fura-2 AM/mag-fura-2 AM. The conventional/real-time quantitative RT-PCR, Western blot and immunocytochemistry were applied. Small interfering RNA (siRNA) for TRPC4 was used to knock down TRPC4. Result: SAA/LPC increased [Ca2+]i by Ca2+ entry. The SAA-induced Ca2+ entry was inhibited by Gd3+, SKF96365 and 2-aminoethoxydiphenyl borate (2-APB), but not nifedipine. The LPC-induced Ca2+ entry was blocked by Gd3+, but not nifedipine, SKF96365 and 2-APB. U73122 and PTX prevented the activation of SAA-, but not LPC-induced Ca2+ influx. LPC, but not SAA, increased [Mg2+]i. The RT-PCR, Western blot and immunocytochemistry of TRP channels revealed the expression of TRPC1/4, TRPV1/2/4 and TRPM7. In siRNA treated cells, the level of TRPC4 mRNA was reduced, and Ca2+ response for SAA was attenuated, compared with control cells. Conclusion: These results suggest that SAA/LPC activate Ca2+ influx in hCASMCs; SAA activates it via PTX-sensitive G-protein, PLC and TRPC pathways, where TRPC4 may be involved. On the other hand, LPC may activate it independently of these pathways. TRP protein may be a target molecule of Ca2+ signaling in hCASMCs elicited by SAA/LPC, which may play roles in coronary muscle remodeling under the pathophysiological conditions such as atherosclerosis. | |||||
書誌情報 | 発行日 2011-03-24 | |||||
日本十進分類法 | ||||||
主題 | 490 | |||||
主題Scheme | NDC | |||||
学位名 | ||||||
学位名 | 博士(医学) | |||||
学位 | ||||||
値 | doctoral | |||||
学位分野 | ||||||
Medical Science(医学) | ||||||
学位授与機関 | ||||||
学位授与機関名 | University of Tokyo (東京大学) | |||||
研究科・専攻 | ||||||
Department of Internal Medicine, Graduate School of Medicine (医学系研究科内科学専攻) | ||||||
学位授与年月日 | ||||||
学位授与年月日 | 2011-03-24 | |||||
学位授与番号 | ||||||
学位授与番号 | 甲第27057号 | |||||
学位記番号 | ||||||
博医第3667号 |