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Wondonin, a novel compound, inhibits hypoxia‐induced angiogenesis through hypoxia‐inducible factor 1 alpha
Author(s) -
Jun Hyoung-Oh,
Kim Younghwa,
Kwon Yoo-Wook,
Hong Soon-Sun,
Kim Kyu-Won,
Shin Jongheon,
Kim Tae-Yoon
Publication year - 2007
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2007.09.034
Subject(s) - angiogenesis , hif1a , hypoxia (environmental) , cd31 , in vivo , in vitro , chemistry , vascular endothelial growth factor , transcription factor , cell culture , cancer research , microbiology and biotechnology , pharmacology , biology , vegf receptors , biochemistry , gene , genetics , organic chemistry , oxygen
Hypoxia regulates a variety of transcription factors including HIF‐1, which has been considered a target for anti‐angiogenic therapy. While searching for a novel anti‐angiogenic agent that would inhibit HIF‐1 activity, we identified wondonin, a new bis imidazole purified from an association of the sponges Poecillastra wondoensis . Wondonin significantly decreased hypoxia‐induced HIF‐1α protein and VEGF expression and inhibited angiogenesis in vitro and in vivo. Furthermore, wondonin down‐regulated HIF‐1α protein through the increased interaction with the pVHL in immortalized human keratinocyte cell line. Wondonin also decreased the immunoreactivities of CD31 and VEGF in epidermal hyperplasia in mice. Taken together, these results suggested that wondonin had the potential to become the anti‐angiogenic therapeutic agent to target HIF‐1α.