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Amelioration of sepsis by TIE2 activation-induced vascular protection

Authors
Han, SangyeulLee, Seung-JunKim, Kyung EunLee, Hyo SeonOh, NuriPark, InwonKo, EunOh, Seung JaLee, Yoon-SookKim, DavidLee, SeungjooLee, Dae HyunLee, Kwang-HoonChae, Su YoungLee, Jung-HoonKim, Su-JinKim, Hyung-ChanKim, SeokkyunKim, Sung HyunKim, ChunghoNakaoka, YoshikazuHe, YulongAugustin, Hellmut G.Hu, JunhaoSong, Paul H.Kim, Yong-InKim, PilhanKim, InjuneKoh, Gou Young
Issue Date
20-4월-2016
Publisher
AMER ASSOC ADVANCEMENT SCIENCE
Citation
SCIENCE TRANSLATIONAL MEDICINE, v.8, no.335
Indexed
SCIE
SCOPUS
Journal Title
SCIENCE TRANSLATIONAL MEDICINE
Volume
8
Number
335
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/88908
DOI
10.1126/scitranslmed.aad9260
ISSN
1946-6234
Abstract
Protection of endothelial integrity has been recognized as a frontline approach to alleviating sepsis progression, yet no effective agent for preserving endothelial integrity is available. Using an unusual anti-angiopoietin 2 (ANG2) antibody, ABTAA (ANG2-binding and TIE2-activating antibody), we show that activation of the endothelial receptor TIE2 protects the vasculature from septic damage and provides survival benefit in three sepsis mouse models. Upon binding to ANG2, ABTAA triggers clustering of ANG2, assembling an ABTAA/ANG2 complex that can subsequently bind and activate TIE2. Compared with a conventional ANG2-blocking antibody, ABTAA was highly effective in augmenting survival from sepsis by strengthening the endothelial glycocalyx, reducing cytokine storms, vascular leakage, and rarefaction, and mitigating organ damage. Together, our data advance the role of TIE2 activation in ameliorating sepsis progression and open a potential therapeutic avenue for sepsis to address the lack of sepsisspecific treatment.
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