Brain‐derived neurotrophic factor promotes angiogenic tube formation through generation of oxidative stress in human vascular endothelial cells

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  • T. Usui
    Laboratory of Veterinary Pharmacology School of Veterinary Medicine Kitasato University Towada Aomori Japan
  • A. Naruo
    Laboratory of Veterinary Pharmacology School of Veterinary Medicine Kitasato University Towada Aomori Japan
  • M. Okada
    Laboratory of Veterinary Pharmacology School of Veterinary Medicine Kitasato University Towada Aomori Japan
  • Y. Hayabe
    Laboratory of Veterinary Pharmacology School of Veterinary Medicine Kitasato University Towada Aomori Japan
  • H. Yamawaki
    Laboratory of Veterinary Pharmacology School of Veterinary Medicine Kitasato University Towada Aomori Japan

書誌事項

公開日
2014-03-10
資源種別
journal article
権利情報
  • http://onlinelibrary.wiley.com/termsAndConditions#vor
DOI
  • 10.1111/apha.12249
公開者
Wiley

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説明

<jats:title>Abstract</jats:title><jats:sec><jats:title>Aim</jats:title><jats:p>Brain‐derived neurotrophic factor (BDNF), a major type of neurotrophins, plays a role in the regulation of synaptic function. Recent studies suggest that BDNF promotes angiogenesis through its specific receptor, tropomyosin‐related kinase B (TrkB). However, the detailed mechanisms for this still remain to be determined. Reactive oxygen species (ROS) generation contributes to the regulation of angiogenesis. Thus, we investigated the mechanisms by which BDNF regulates angiogenesis with focusing on ROS in cultured human vascular endothelial cells (ECs).</jats:p></jats:sec><jats:sec><jats:title>Methods and results</jats:title><jats:p>In human umbilical vein ECs, BDNF increased ROS generation as measured fluorometrically using 2′ 7′‐dichlorofluorescein diacetate as well as NADPH oxidase (NOX) activity as measured by lucigenin assay. BDNF‐induced ROS generation and NOX activity were inhibited by K252a, a TrkB receptor inhibitor. BDNF induced phosphorylation of p47 phox, a regulatory component of NOX, which was inhibited by K252a as measured by Western blotting. BDNF increased angiogenic tube formation in ECs, which was completely inhibited by K252a or gp91ds‐tat, a NOX inhibitor. BDNF caused Akt phosphorylation in ECs, which was inhibited by K252a or gp91ds‐tat.</jats:p></jats:sec><jats:sec><jats:title>Conclusion</jats:title><jats:p>The present results for the first time demonstrate that BDNF induces NOX‐derived ROS generation through activation of p47 phox in a TrkB receptor‐dependent manner, which leads to the promotion of angiogenic tube formation possibly via Akt activation.</jats:p></jats:sec>

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