The targeted delivery of the c-Src peptide complexed with schizophyllan to macrophages inhibits polymicrobial sepsis and ulcerative colitis in mice
- Authors
- Kim, Ye-Ram; Hwang, Jangsun; Koh, Hyun-Jung; Jang, Kiseok; Lee, Jong-Dae; Choi, Jonghoon; Yang, Chul-Su
- Issue Date
- May-2016
- Publisher
- Pergamon Press Ltd.
- Keywords
- Schizophyllan; c-Src; Reactive oxygen species; Sepsis; Colitis
- Citation
- Biomaterials, v.89, pp 1 - 13
- Pages
- 13
- Indexed
- SCI
SCIE
SCOPUS
- Journal Title
- Biomaterials
- Volume
- 89
- Start Page
- 1
- End Page
- 13
- URI
- https://scholarworks.bwise.kr/erica/handle/2021.sw.erica/13702
- DOI
- 10.1016/j.biomaterials.2016.02.035
- ISSN
- 0142-9612
1878-5905
- Abstract
- Hyper-inflammatory responses triggered by intracellular reactive oxygen species (ROS) can lead to a variety of diseases, including sepsis and colitis. However, the regulators of this process remain poorly defined. In this study, we demonstrate that c-Src is a negative regulator of cellular ROS generation through its binding to p47phox. This molecule also competitively inhibits the NADPH oxidase complex (NOX) assembly. Furthermore, we developed the schizophyllan (SPG)-c-Src SH3 peptide, which is a beta-1,3-glucan conjugated c-Src SH3-derived peptide composed of amino acids 91-108 and 121-140 of c-Src. The SPG-SH3 peptide has a significant therapeutic effect on mouse ROS-mediated inflammatory disease models, cecal-ligation puncture-induced sepsis, and dextran sodium sulfate-induced colitis. It does so by inhibiting the NOX subunit assembly and proinflammatory mediator production. Therefore, the SPG-SH3 peptide is a potential therapeutic agent for ROS-associated lethal inflammatory diseases. Our findings provide clues for the development of new peptide-base drugs that will target p47phox. (C) 2016 Elsevier Ltd. All rights reserved.
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