亜鉛トランスポーターZIP12は慢性低酸素に対する肺血管反応を調節する
Lan Zhao1, Eduardo Oliver1, Klio Maratou2
1Centre for Pharmacology and Therapeutics, Division of Experimental Medicine, Imperial College London, Hammersmith Hospital, London W12 0NN, UK.
Nature
|August 11, 2015
まとめ
研究者らは,亜鉛トランスポーターZIP12 (Slc39a12) を低酸素誘発性肺高血圧の重要な因子として特定した. ZIP12を阻害することで,この状態に対する新しい治療法が提供される可能性があります.
科学分野:
- 生理学
- 遺伝学
- 薬理学について
背景:
- 哺乳類の肺循環は酸素不足で通常収縮して再構成され,肺高血圧と右心房高縮を引き起こします.
- いくつかの哺乳類は,低酸素誘発性肺高血圧に対する遺伝的抵抗性を有しており,これは基本的な規制メカニズムを示しています.
研究 の 目的:
- 低酸素誘発性肺血管改造を制御する遺伝的要因を特定する.
- 肺高血圧における亜鉛トランスポーターZIP12の役割を調査する.
主な方法:
- 遺伝的繁殖プログラムとネズミの比較ゲノム
- 感受性の高い哺乳類 (ネズミ,牛,人間) のZIP12発現の分析
- 肺血管の滑らかな筋肉の細胞に関する in vitro 研究と,低酸素ラットにおける in vivo 研究.
主要な成果:
- ZIP12をコードするSlc39a12は,低酸素誘発性肺血管改造の主なレギュラーとして特定されました.
- 感受性の高い哺乳類の肺動脈でZIP12発現が増加し,滑らかな筋肉細胞では低酸素依存であった.
- ZIP12抑制は細胞内亜鉛と滑らかな筋肉細胞の増殖を減少させ,遺伝的障害はネズミの肺高血圧を弱めた.
結論:
- ZIP12は哺乳類の肺血管の恒常性において基本的な役割を果たします.
- ZIP12をターゲットにすることで,肺高血圧の管理に新しい治療法が提供されます.
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