東邦大学 教育・研究業績データベース   
     


  イトウ マサノリ   Ito Masanori
  伊藤 雅方
   所属   東邦大学  医学部 医学科
   職種   講師
言語種別 英語
発表タイトル Altered expression of Ca2+-signaling proteins in atria and pulmonary vein of DM model mice.
会議名 The 89th Annual Meeting of The Japanese Pharmacological Society
学会分類 日本医学会
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, Sugimoto Y, Seki Y, Tomida T, Adachi-Akahane S
発表年月日 2016/03/09
開催地
(都市, 国名)
横浜
概要 Diabetes mellitus (DM) and obesity are risk factors of developing atrial fibrillation (AF) in aged populations. AF involves structural and electrical remodeling associated with abnormal Ca2+signaling in pulmonary veins (PV) and atrial substrates. Electrical remodeling is characterized by the reduction of refractory period due to a shortening of APD in atrial myocytes. However, changes in expression and localization of Ca2+ signaling proteins have not been extensively studied in PV and atria of DM model mice. In the present study, we studied the expression and localization of Ca2+ signaling proteins in atria and PV, in comparison with ventricle, in type 1 DM model mice. [Methods] DM was induced in C57BL/6J mice (male, 8-week-old) by a single injection of streptozotocin (STZ, 180 mg/kg, i.p.). Hyperglycemia was confirmed by a blood glucose test. Experiments were carried out four weeks after injection of STZ. [Results & Discussion] qRT-PCR and immunohistochemistry revealed that L-type Ca2+ channel CaV1.3 is highly expressed in PV (PV > atria >> ventricle). mRNA levels of β2-AR and β3-AR as well as IP3R were also markedly high in PV. In atria of DM mice, mRNA levels of CaV1.3, junctophilin-2, and RyR2 were significantly lower than those of vehicle controls. These results suggest that down-regulation of Ca2+ signaling proteins are involved in raising the risk of AF in DM.