Journal article
Action of epoxyeicosatrienoic acids on cellular function
American Journal of Physiology: Cell Physiology, Vol.292(3), pp.C996-1012
03/2007
DOI: 10.1152/ajpcell.00402.2006
PMID: 16987999
Abstract
Epoxyeicosatrienoic acids (EETs), which function primarily as autocrine and paracrine mediators in the cardiovascular and renal systems, are synthesized from arachidonic acid by cytochrome P-450 epoxygenases. They activate smooth muscle large-conductance Ca(2+)-activated K(+) channels, producing hyperpolarization and vasorelaxation. EETs also have anti-inflammatory effects in the vasculature and kidney, stimulate angiogenesis, and have mitogenic effects in the kidney. Many of the functional effects of EETs occur through activation of signal transduction pathways and modulation of gene expression, events probably initiated by binding to a putative cell surface EET receptor. However, EETs are rapidly taken up by cells and are incorporated into and released from phospholipids, suggesting that some functional effects may occur through a direct interaction between the EET and an intracellular effector system. In this regard, EETs and several of their metabolites activate peroxisome proliferator-activated receptor alpha (PPARalpha) and PPARgamma, suggesting that some functional effects may result from PPAR activation. EETs are metabolized primarily by conversion to dihydroxyeicosatrienoic acids (DHETs), a reaction catalyzed by soluble epoxide hydrolase (sEH). Many potentially beneficial actions of EETs are attenuated upon conversion to DHETs, which do not appear to be essential under routine conditions. Therefore, sEH is considered a potential therapeutic target for enhancing the beneficial functions of EETs.
Details
- Title: Subtitle
- Action of epoxyeicosatrienoic acids on cellular function
- Creators
- Arthur A Spector - University of IowaAndrew W Norris
- Resource Type
- Journal article
- Publication Details
- American Journal of Physiology: Cell Physiology, Vol.292(3), pp.C996-1012
- DOI
- 10.1152/ajpcell.00402.2006
- PMID
- 16987999
- ISSN
- 0363-6143
- eISSN
- 1522-1563
- Grant note
- HL072845 / NHLBI NIH HHS DK064906 / NIDDK NIH HHS K08 DK064906 / NIDDK NIH HHS
- Language
- English
- Date published
- 03/2007
- Academic Unit
- Endocrinology and Diabetes; Stead Family Department of Pediatrics; Biochemistry and Molecular Biology; Internal Medicine
- Record Identifier
- 9984293073302771
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