非共振結合から共振結合への変換によるペプチドアンフィフィルのプログラム可能な組立
Kohei Sato, Wei Ji1, Liam C Palmer
1Prometheus, Division of Skeletal Tissue Engineering, and ∥Skeletal Biology and Engineering Research Center, Department of Development and Regeneration, KU Leuven , Leuven 3000, Belgium.
Journal of the American Chemical Society
|June 23, 2017
まとめ
研究者はペプチドアンフィフィールモノマー間の共性結合を形成することによって,超分子ポリマー長さを制御した. より長いナノファイバーは 細胞の活性を高め 生物医学的な応用の可能性を示唆した.
科学分野:
- 超分子化学
- 材料科学
- バイオ材料工学
背景:
- 超分子ポリマーのモノマー数を制御することは,プログラム可能な自己組み立てに困難です.
- 分子間の力を調整することで 挫折した成長は アセンブリのサイズを制限する 戦略のひとつです
- ペプチドアンフィフィルは,自己組み立てナノ構造のための多用途のプラットフォームを提供します.
研究 の 目的:
- 超分子ナノファイバーの長さを制御するメカニズムとして共性結合形成を調査する.
- 潜在的生物医学的な応用のための細胞毒性に対する繊維長さの影響を評価する.
主な方法:
- ペプチド・アンフィフィルの自己組織化が続いて,共価結合が形成される.
- 円形二重光学,ダイナミック光散乱,サイズ除外クロマトグラフィ,構造分析のための伝送電子顕微鏡.
- C2C12プレミオブラスト細胞を用いた細胞毒性測定
主要な成果:
- 結合結合形成は静電抵抗を補償し 制御された繊維の伸びを可能にします
- ペプチドナノファイバー内の水素結合は,共振交絡によって強化された.
- 細胞活性はナノファイバーの長さを増加させ,細胞毒性の低下を示した.
結論:
- 協和結合形成は,超分子ナノファイバーの長さを制御する効果的な戦略です.
- より長いペプチドアンフィフィールナノファイバーは,安定したエンドキャップのために,細胞毒性が低下しています.
- これらの発見は,生物医学アプリケーションのためのペプチドアンフィフィールナノファイバーの開発をサポートします.
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