TY - JOUR
T1 - 11,12-Epoxyeicosatrienoic acid stimulates heme-oxygenase-1 in endothelial cells
AU - Sacerdoti, David
AU - Colombrita, Claudia
AU - Di Pascoli, Marco
AU - Schwartzman, Michal L.
AU - Bolognesi, Massimo
AU - Falck, John R.
AU - Gatta, Angelo
AU - Abraham, Nader G.
N1 - Funding Information:
This work was supported by NIH grants HL55601 and HL34300 (NGA) and GM31278 (JRF) a grant from the Italian Ministry for University and Scientific and Technological Research (MURST).
PY - 2007/1
Y1 - 2007/1
N2 - As epoxyeicosatrienoic acids (EETs), particularly 11,12-EET, and the heme oxygenase/carbon monoxide (HO/CO) system share overlapping biological activities, we examined a possible link between 11,12-EET and HO activity in endothelial cells. Confocal microscopy analysis of immunostaining of HO-1 and HO-2 in cultured endothelial cells treated with 11,12-EET (1 μM) showed an increase in florescence of HO-1 protein in the various cellular compartments, but not of HO-2. Incubation of endothelial cells with 11,12-EET (1 μM) for 24 h increased the level of HO-1 protein by about three-fold. Similarly, incubation of endothelial cells with 8,9-EET and sodium nitroprussiate, a known inducer of HO-1, increased HO-1 protein without any effect on HO-2. Upregulation of HO-1 by 11,12-EET, as well as 8,9-EET, was associated with an increase in HO activity, which was inhibited by stannous mesoporphirin (10 μM). Incubation of rat aortas with 11,12-EET (1 μM for 60 min) increased HO activity. These findings identify a novel effect of EETs on endothelial HO-1 and indicate that the signaling pathway of EETs in endothelial cells is possibly via an increase in HO-1 expression and activity.
AB - As epoxyeicosatrienoic acids (EETs), particularly 11,12-EET, and the heme oxygenase/carbon monoxide (HO/CO) system share overlapping biological activities, we examined a possible link between 11,12-EET and HO activity in endothelial cells. Confocal microscopy analysis of immunostaining of HO-1 and HO-2 in cultured endothelial cells treated with 11,12-EET (1 μM) showed an increase in florescence of HO-1 protein in the various cellular compartments, but not of HO-2. Incubation of endothelial cells with 11,12-EET (1 μM) for 24 h increased the level of HO-1 protein by about three-fold. Similarly, incubation of endothelial cells with 8,9-EET and sodium nitroprussiate, a known inducer of HO-1, increased HO-1 protein without any effect on HO-2. Upregulation of HO-1 by 11,12-EET, as well as 8,9-EET, was associated with an increase in HO activity, which was inhibited by stannous mesoporphirin (10 μM). Incubation of rat aortas with 11,12-EET (1 μM for 60 min) increased HO activity. These findings identify a novel effect of EETs on endothelial HO-1 and indicate that the signaling pathway of EETs in endothelial cells is possibly via an increase in HO-1 expression and activity.
KW - 11,12-EET
KW - CO
KW - Carbon monoxide
KW - Endothelial cell
KW - Epoxygenase
KW - HO-1
KW - Heme oxygenase
UR - http://www.scopus.com/inward/record.url?scp=33845317918&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=33845317918&partnerID=8YFLogxK
U2 - 10.1016/j.prostaglandins.2006.07.001
DO - 10.1016/j.prostaglandins.2006.07.001
M3 - Article
C2 - 17164143
AN - SCOPUS:33845317918
SN - 1098-8823
VL - 82
SP - 155
EP - 161
JO - Prostaglandins and Other Lipid Mediators
JF - Prostaglandins and Other Lipid Mediators
IS - 1-4
ER -