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PKCε-CREB-Nrf2 signalling induces HO-1 in the vascular endothelium and enhances resistance to inflammation and apoptosis
Author(s) -
Hayley Mylroie,
Odile Dumont,
Andrea S. Bauer,
Clare Thornton,
John B. G. Mackey,
Damien Calay,
Shahir Hamdulay,
Joan Choo,
Joseph J. Boyle,
Allen M. Samarel,
Anna M. Randi,
Paul C. Evans,
Justin C. Mason
Publication year - 2015
Publication title -
cardiovascular research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.774
H-Index - 219
eISSN - 1755-3245
pISSN - 0008-6363
DOI - 10.1093/cvr/cvv131
Subject(s) - creb , protein kinase c , rottlerin , apoptosis , microbiology and biotechnology , endothelial dysfunction , signal transduction , inflammation , biology , endothelium , endocrinology , medicine , cancer research , chemistry , immunology , transcription factor , biochemistry , gene
Vascular injury leading to endothelial dysfunction is a characteristic feature of chronic renal disease, diabetes mellitus, and systemic inflammatory conditions, and predisposes to apoptosis and atherogenesis. Thus, endothelial dysfunction represents a potential therapeutic target for atherosclerosis prevention. The observation that activity of either protein kinase C epsilon (PKCε) or haem oxygenase-1 (HO-1) enhances endothelial cell (EC) resistance to inflammation and apoptosis led us to test the hypothesis that HO-1 is a downstream target of PKCε.

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