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Selective activation of NADPH oxidase subunit 2 (NOX2) by A3 adenosine receptor in mouse aorta
Author(s) -
ElAwady Mohammed S.,
Ansari Habib R,
Fil Daniel,
Tilley Stephen L,
Mustafa S. Jamal
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.lb366
Subject(s) - nox4 , nox1 , apocynin , nadph oxidase , chemistry , adenosine , medicine , nad(p)h oxidase , agonist , endocrinology , reactive oxygen species , receptor , biochemistry , biology
The NADPH oxidase (NOX) subunits 1, 2 and 4 are the major sources for reactive oxygen species (ROS) in vascular tissue. We have shown earlier that activation of A 3 adenosine receptor (A 3 AR) leads to contraction of aorta as well a decrease in coronary flow (Talukder, et al. , 2002; Ansari, et al. , 2007). In conditions such as ischemia‐reperfusion and hypoxia, both ROS and adenosine are released suggesting a possible interaction. Our aim in this study was to examine the relationship between A 3 AR and NOX1, NOX2 (gp91 phox ) and NOX4 in mouse aorta. The protein and mRNA expression of the NOX1, NOX2 and NOX4 were measured in aortic rings from WT and A 3 AR knockout (A 3 KO) mice. A 3 AR agonist Cl‐IBMECA (10 −7 M) was used in the presence or absence of the NOX inhibitor (apocynin, 10 −5 M). Cl‐IBMECA selectively increased protein expression of NOX2 by 150±15% in WT but not in A 3 KO mouse aortas and this increase was inhibited by apocynin. Neither NOX1 nor NOX4 protein expressions were affected by Cl‐IBMECA. Interestingly, the mRNA of NOX2 was not changed by Cl‐IBMECA in either WT or A 3 KO aortas, suggesting that NOX2 protein increase by Cl‐IBMECA may be through either a change in protein translation or turnover. In conclusion, A 3 AR selectively activates NOX2 without affecting NOX1 or NOX4 in mouse aorta, suggesting a role for NOX2 in adenosine mediated control of vascular tone through A 3 AR (Supported by NIH grants HL 027339, HL 094447, HL071802).