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持続時間に依存しないインスリン/IGF-1シグナリングは,長寿におけるコラーゲンリモデリングを意味する

Collin Y Ewald¹, Jess N Landis², Jess Porter Abate¹

¹1] Joslin Diabetes Center, One Joslin Place, Boston, Massachusetts 02215, USA [2] Harvard Stem Cell Institute, 7 Divinity Avenue, Cambridge, Massachusetts 02138, USA [3] Department of Genetics, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, Massachusetts 02215, USA.

|December 18, 2014

まとめ

減少したインスリン/IGF-1シグナル伝達 (rIIS) は,SKN-1を利用してコラーゲン生成を促進し,長寿のために細胞外マトリクスの若さを維持するために,Dauerから独立した経路を通じてC. elegansの寿命を延長します.

科学分野:

ゲロントロジーはゲロントロジーの学科です.
分子生物学は分子生物学である.
バイオケミストリーバイオケミストリー

背景:

老化には,細胞損傷と細胞外マトリックス (ECM) の衰退が伴う.
減少したインスリン/IGF-1シグナル伝達 (rIIS) は寿命を延ばしますが,そのECM効果は不明です.
dauer経路は,rIISの寿命延長に関連していますが,代替メカニズムがあります.

研究の目的:

rIISが老化中のECMにどのように影響するか調査する.
期間に関係なく老化経路を特定する.
rIISによる長寿とECMのメンテナンスにおけるSKN-1の役割を調査する.

主な方法:

モデル生物としてCaenorhabditis elegansを使用しました.
rIIS,DAF-16,SKN-1経路を研究するために遺伝子操作を行いました.
コラーゲンとECM成分に焦点を当てて,遺伝子発現を分析した.
様々な遺伝的および環境条件下で評価された寿命.

主要な成果:

rIISは,SKN-1を対象とした,ダイアから独立した経路を通じて,C. elegansの長寿を促進します.
SKN-1は,ダウアー特征のない低IISによって活性化されると,コラーゲンとECMの遺伝子発現をアップレギュレーションします.
長寿を促す様々な介入は,年齢に関連したコラーゲン発現の低下を遅らせます.
コラーゲン媒介によるECMリモデリエーションは,持続時間独立のrIIS経路の寿命延長に不可欠です.

結論:

IISは,成人のC. elegans. の様々な保護機構を調節する.
SKN-1とECMのリモデリングを含むダイアル独立経路は,長寿に寄与する.
ECMの若さを維持することは,様々なアンチエイジング介入の有効性にとって極めて重要です.

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