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Hypoxia-induced pulmonary hypertension: comparison of soluble epoxide hydrolase deletion vs. inhibition
Author(s) -
Benjamin Keserü,
Eduardo BarbosaSicard,
Ralph T. Schermuly,
Hiromasa Tanaka,
Bruce D. Hammock,
Norbert Weißmann,
Beate Fißlthaler,
Ingrid Fleming
Publication year - 2009
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/cvp281
Subject(s) - epoxide hydrolase 2 , hypoxia (environmental) , pulmonary hypertension , epoxide hydrolase , medicine , chemistry , cardiology , endocrinology , pharmacology , biochemistry , biology , enzyme , oxygen , organic chemistry , microsome
The C-terminal domain of the soluble epoxide hydrolase (sEH) metabolizes epoxyeicosatrienoic acids (EETs) to their less active diols, while the N-terminal domain demonstrates lipid phosphatase activity. As EETs are potent vasoconstrictors in the pulmonary circulation, we assessed the development of pulmonary hypertension induced by exposure to hypoxia (10% O(2)) for 21 days in wild-type (WT) and sEH(-/-) mice and compared the effects with chronic (4 months) sEH inhibition.

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