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KAKEN_16K19367seika.pdf
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Title |
Title |
腸管自然リンパ球における腸管特異性規定遺伝子の役割
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チョウカン シゼン リンパキュウ ニ オケル チョウカン トクイセイ キテイ イデンシ ノ ヤクワリ
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Chōkan shizen rinpakyū ni okeru chōkan tokuisei kitei idenshi no yakuwari
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The role of Nr4a3 on intestinal homeostasis
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佐伯, 恵太
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サエキ, ケイタ
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Saeki, Keita
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慶應義塾大学・医学部・特任助教
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科研費研究者番号 : 80528729
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吉村, 昭彦
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ヨシムラ, アキヒコ
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Yoshimura, Akihiko
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慶應義塾大学・医学部・教授
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Research team member
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科研費研究者番号 : 90182815
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2018
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科学研究費補助金研究成果報告書
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2017
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当研究ではNr4a3分子に着目しその腸管恒常性制御につき検討した。ヒトNr4a3遺伝子はヒルシュスプルング病の病因未同定領域である9q31領域に存在し, Nr4a3欠損マウスはヒルシュスプルング病類似疾患様の病態をとり, 腸管神経叢が低形成になることが判明した。さらに, Nr4a3欠損マウスは急性腸炎抵抗性であり, 一部のセロトニン受容体作動薬によりその差が解消され, 消化管神経叢と急性腸炎の新たな制御メカニズムを見出すことに成功した。当研究は過去に報告を見ない消化管神経節形成を介した急性炎症制御メカニズムに迫り, 新たな診断ならびに治療応用への突破口になるものと思われる。
We focused on Nr4a3 orphan receptor and how it regulates intestinal homeostasis. Human Nr4a3 gene is located on chromosome 9q31.1 region where the unidentified causative gene of Hirschsprung disease is. In absence of Nr4a3 in mice, the colon has hypoplastic ganglia in its myenteron and wriggles more slowly than wild type. Furthermore, Nr4a3-deficient mice are resistant to dextran sodium sulfate induced acute colitis. This resistance is partially cancelled by giving 5-HT1A agonist and calcitonin gene related peptide seems to be a key regulator for this. Our findings demonstrate novel mechanism of neuro-gut axis in gut motility and inflammation and make a breakthrough in the diagnosis of HSCR subtypes and therapy for novel intestinal inflammatory diseases.
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研究種目 : 若手研究(B)
研究期間 : 2016~2017
課題番号 : 16K19367
研究分野 : 医歯 薬学 内科系臨床医学 消化器内科学 8202
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