アカハネ サトミ
Adachi-Akahane Satomi
赤羽 悟美 所属 東邦大学 医学部 医学科 職種 教授 |
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言語種別 | 英語 |
発表タイトル | Novel role of lipid binding protein in the regulation of excitability in atrial myocytes. |
会議名 | The 6th Joint Seminor on Biomedical Sciences |
学会区分 | 国内学会 |
発表形式 | ポスター掲示 |
講演区分 | 一般 |
発表者・共同発表者 | ◎Ito M†, Izumi-Nakaseko H†, Tsuru H†, Adachi-Akahane S† |
発表年月日 | 2009/10/12 |
開催地 (都市, 国名) |
Tokyo |
概要 | Recent studies have shown that the impairment of L-type Ca2+ channel function is associated with arrhythmia such as atrial fibrillation. In addition to modulation of ion channel activities, manipulation of lipid metabolism system has been shown to be a novel strategy for the treatment of atrial fibrillation. We identified phosphatidylcholine transfer protein-like protein (PCTP-L/StarD10) as a protein interacting with the C-terminal region of voltage dependent L-type calcium channel α1C subunit (CaV1.2) by yeast two hybrid screening. The functional role of PCTP-L/StarD10 has been unknown, although M\mammalian START family proteins (STARD1-15) have been shown to be involved in lipid transfer between intracellular compartments, lipid metabolism, and modulation of signaling events. The patch-clamp study demonstrated that PCTP-L/StarD10 modulates the voltage-dependent inactivation of L-type Ca2+ channels through the subtype-specific interaction with CaV1.2, and thus maintains the availability of L-type Ca2+ channels. The knockdown of PCTP-L/StarD10 in cultured neonatal atrial myocytes resulted in the shortening of action potential duration and an increase in the frequency of spontaneous action potentials. These results indicate that the excitability of atrial myocytes is regulated through signaling complex that involves the L-type Ca2+ channel and PCTP-L/StarD10. |