The epoxy fatty acid pathway enhances cAMP in mammalian cells through multiple mechanisms

被引:0
作者
Matsumoto, Naoki [1 ,2 ]
Singh, Nalin [1 ,2 ]
Lee, Kin Sing [3 ]
Barnych, Bogdan [1 ,2 ]
Morisseau, Christophe [1 ,2 ]
Hammock, Bruce D. [1 ,2 ]
机构
[1] Univ Calif Davis, Dept Entomol & Nematol, One Shields Ave, Davis, CA 95616 USA
[2] Univ Calif Davis, Comprehens Canc Ctr, Davis, CA USA
[3] Michigan State Univ, Dept Pharmacol & Toxicol, E Lansing, MI USA
关键词
Eicosanoid; Epoxyeicosatrienoicacid; Dihydroxyeicosatrienoicacid; Solubleepoxidehydrolase; CyclicAMP; EP2; Inflammation; RAM SEMINAL-VESICLES; SMOOTH-MUSCLE; 11,12-EPOXYEICOSATRIENOIC ACID; 14,15-EPOXYEICOSATRIENOIC ACID; PHARMACOLOGICAL INHIBITION; DOCOSAHEXAENOIC ACID; HYDROLASE DEFICIENCY; INDUCED LIPOKINE; TUMOR-GROWTH; HUMAN PLASMA;
D O I
10.1016/j.prostaglins.2022.106662
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The cellular mechanism by which epoxy fatty acids (EpFA) improves disease status is not well characterized. Previous studies suggest the involvement of cellular receptors and cyclic AMP (cAMP). Herein, the action of EpFAs derived from linoleic acid (LA), arachidonic acid (ARA), and docosahexaenoic acid on cAMP levels was studied in multiple cell types to elucidate relationships between EpFAs, receptors and cells' origin. cAMP levels were enhanced in HEK293 and LLC-PK1 cells by EpFAs from LA and ARA. Using selective antagonists, the EpFA effects on cAMP levels appear dependent on the prostaglandin E2 receptor 2 (EP2) but not 4 (EP4). Human coronary artery smooth muscle cells responded similarly to the EpFAs. However, we were not able to show the involvement of any of the receptors tested in this cell type. The results pinpointed distinct cell lines and receptor subtypes that natively respond to EpFA.
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页数:8
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