ストロマルR-スポンジンは胃上皮幹細胞と腺の恒常性を調整する
Michael Sigal1,2,3, Catriona Y Logan4, Marta Kapalczynska1,2
1Department of Molecular Biology, Max Planck Institute for Infection Biology, 10117 Berlin, Germany.
Nature
|August 17, 2017
まとめ
胃幹細胞の循環は,Wntシグナル伝達とR-スポンディン3によって調節される. ヘリコバクター・パイロリ感染症は 幹細胞の増殖を促し 胃上皮の再生や増殖を引き起こします
科学分野:
- 胃腸内科
- 幹細胞生物学
- 再生医療
背景:
- 胃上皮の再生は長寿の幹細胞に依存していますが 制御メカニズムは不明です
- Wnt信号は幹細胞のアイデンティティと上皮の再生に不可欠です.
- ヘリコバクター・パイロリ感染は胃幹細胞を活性化し,上皮の周回を増加させます.
研究 の 目的:
- 胃幹細胞の循環の調節を調査する
- 胃再生におけるWntシグナル伝達とストロマル因子の役割を明らかにする.
- 胃幹細胞の動態に対するヘリコバクター・パイロリの影響を理解する.
主な方法:
- 胃腺のWnt信号マーカー (Axin2) と幹細胞マーカー (Lgr5) の分析
- 胃のミオフィブロブラストにおけるR-スポンディン3の発現と機能の調査
- R- スポンジンの投与とH. pylori感染後の幹細胞増殖と腺再生の評価
主要な成果:
- Axin2によって標識されたWnt信号は,幹細胞のニッチに局所されています.
- Lgr5+幹細胞と隣接するLgr5細胞は,Axin2を発現し,腺の再生に寄与する.
- ミオフィブロブラストによって生成されるストロマルR-スポンディン3は,Axin2とLgr5発現に不可欠である.
- H. pyloriの感染は,ストロマのR-スポンディン3を調節し,Axin2+細胞群を拡大し,腺増殖を引き起こします.
結論:
- 胃上皮幹細胞のダイナミクスを制御するストロマルニッチ細胞は,R-スポンディン3を通じます.
- この相互作用は上皮の再生を指揮し,組織の完全性を維持します.
- H. pyloriは このメカニズムを利用して 増殖と増殖を引き起こします
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