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KAKEN_26461619seika.pdf
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Title |
Title |
肺動脈性高血圧症の進展を抑制する細胞内カルシウムシグナルの解明
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Kana |
ハイドウミャクセイ コウケツアツショウ ノ シンテン オ ヨクセイスル サイボウナイ カルシウム シグナル ノ カイメイ
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Romanization |
Haidomyakusei koketsuatsusho no shinten o yokuseisuru saibonai karushiumu shigunaru no kaimei
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Intracellular calcium signals inhibiting the progression of pulmonary arterial hypertension
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内田, 敬子
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ウチダ, ケイコ
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Uchida, Keiko
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慶應義塾大学・保健管理センター・講師
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Research team head
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科研費研究者番号 : 50286522
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山岸, 敬幸
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ヤマギシ, ヒロユキ
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Yamagishi, Hiroyuki
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慶應義塾大学・医学部小児科・教授
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Research team member
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科研費研究者番号 : 40255500
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御子柴, 克彦
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ミコシバ, カツヒコ
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Mikoshiba, Katsuhiko
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柴田, 映道
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シバタ, アキミチ
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Shibata, Akimichi
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2017
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科学研究費補助金研究成果報告書
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2016
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Abstract |
長期低酸素暴露による肺高血圧症の程度を野生型と2型イノシトール三リン酸受容体(IP3R2)ノックアウト(KO)マウスで比較したところ, 心エコーによる右心機能, 右心室の相対的重量による右室肥大, 肺組織切片における肺動脈中膜肥厚の全てにおいて, KOマウスでは肺高血圧症が増悪していた。IP3R2は肺内では肺動脈平滑筋に特異的に発現しており, 肺動脈平滑筋のアポトーシス抵抗性が亢進し, カルシウム流入分子の一つであるTRPc4の発現が上昇していた。さらに, 単離肺動脈平滑筋細胞初代培養において, ストア感受性Ca2+流入活性が亢進しており, 肺動脈性肺高血圧を増悪させている主な原因経路の一つと考えられた。
Inositol trisphosphate receptor (IP3R) is an intracellular Ca2+ release channel. As we found the strong expression of the type 2 IP3R (IP3R2) in the pulmonary arterial smooth muscle cells (PASMCs), we investigated the contribution of IP3R2 to pathophysiology of PAH. IP3R2 knockout (KO) mice treated with chronic hypoxia showed higher PA pressure and RV pressure than WT mice in echocardiography. RV hypertrophy and medial wall thickness of PASMCs were more severe in KO. There was significant decrease of TUNEL positive cells in KO, suggesting that apoptosis was reduced in KO PASMCs. Ca2+ imaging revealed that SOCE was enhanced in KO compared with WT. Taken together, chronic hypoxia-induced PAH was deteriorated in IP3R2 KO. The deletion of IP3R2 gene led to inhibition of apoptosis and enhanced SOCE in PASMCs, probably resulting in acceleration of the progression of PAH induced by chronic hypoxia.
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研究種目 : 基盤研究(C)(一般)
研究期間 : 2014~2016
課題番号 : 26461619
研究分野 : pediatric cardiology
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