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The Journal of clinical investigation v.127 no.11, 2017년, pp.3987 - 4000   SCI SCIE SCOPUS
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Mast cell hyperactivity underpins the development of oxygen-induced retinopathy

Matsuda, Kenshiro    (Cooperative Major in Advanced Health Science, Graduate School of Bio-Applications and System Engineering, Tokyo University of Agriculture and Technology, Tokyo, Japan.   ); Okamoto, Noriko    (Laboratory of Veterinary Molecular Pathology and Therapeutics, and Division of Animal Life Science, Institute of Agriculture, Tokyo University of Agriculture and Technology, Tokyo, Japan.   ); Kondo, Masatoshi    (Department of Neonatology and Tokyo Metropolitan Children's Medical Center, Tokyo, Japan.   ); Arkwright, Peter D.    (Institute of Inflammation and Repair, University of Manchester, Royal Manchester Children's Hospital, Manchester, United Kingdom.   ); Karasawa, Kaoru    (Cooperative Major in Advanced Health Science, Graduate School of Bio-Applications and System Engineering, Tokyo University of Agriculture and Technology, Tokyo, Japan.   ); Ishizaka, Saori    (Cooperative Major in Advanced Health Science, Graduate School of Bio-Applications and System Engineering, Tokyo University of Agriculture and Technology, Tokyo, Japan.   ); Yokota, Shinichi    (Laboratory of Veterinary Molecular Pathology and Therapeutics, and Divis  ); Matsuda, Akira   Jung, Kyungsook   Oida, Kumiko   Amagai, Yosuke   Jang, Hyosun   Noda, Eiichiro   Kakinuma, Ryota   Yasui, Koujirou   Kaku, Uiko   Mori, Yasuo   Onai, Nobuyuki   Ohteki, Toshiaki   Tanaka, Akane   Matsuda, Hiroshi  
  • 초록  

    Mast cells are classically thought to play an important role in protection against helminth infections and in the induction of allergic diseases; however, recent studies indicate that these cells also contribute to neovascularization, which is critical for tissue remodeling, chronic inflammation, and carcinogenesis. Here, we demonstrate that mast cells are essential for sprouting angiogenesis in a murine model of oxygen-induced retinopathy (OIR). Although mouse strains lacking mast cells did not exhibit retinal neovascularization following hypoxia, these mice developed OIR following infusion of mast cells or after injection of mast cell tryptase (MCT). Relative hypoxia stimulated mast cell degranulation via transient receptor potential ankyrin 1. Subsequent surges in MCT stimulated retinal endothelial cells to produce monocyte chemotactic protein-1 (MCP1) and angiogenic factors, leading to sprouting angiogenesis. Mast cell stabilizers as well as specific tryptase and MCP1 inhibitors prevented the development of OIR in WT mice. Preterm infants with early retinopathy of prematurity had markedly higher plasma MCT levels than age-matched infants without disease, suggesting mast cells contribute to human disease. Together, these results suggest therapies that suppress mast cell activity should be further explored as a potential option for preventing eye diseases and subsequent blindness induced by neovascularization.


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