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Hydrogen peroxide (H 2 O 2 ) is not increased in angiotensin II (AngII)‐stimulated neurons overexpressing superoxide dismutase (SOD)
Author(s) -
Case Adam J,
Cruz Rodrigo Franco,
Zimmerman Matthew C
Publication year - 2013
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.27.1_supplement.1143.15
Subject(s) - angiotensin ii , superoxide dismutase , chemistry , superoxide , stimulation , hydrogen peroxide , signal transduction , downregulation and upregulation , microbiology and biotechnology , enzyme , biochemistry , endocrinology , biology , receptor , gene
Previous studies have shown that SOD overexpression in neurons inhibits AngII intra‐neuronal signaling; thus, suggesting that superoxide radicals (O 2 •− ) are key signaling intermediates driving AngII‐induced neuronal activation. However, considering H 2 O 2 is a direct product of O 2 •− dismutation by SOD, an alternative interpretation is that increased H 2 O 2 mediates the inhibition of AngII signaling in SOD overexpressing neurons. We aimed to determine if H 2 O 2 levels are indeed increased in SOD overexpressing neurons stimulated with AngII. To query this, we used a neuronal cell culture model expressing HyPer, a H 2 O 2 ‐sensitive fluorescent protein. To determine the sensitivity of HyPer to H 2 O 2 , neurons were stimulated with increasing concentrations of H 2 O 2 (1–100 μM) and changes in HyPer fluorescence were observed by real‐time confocal imaging. Robust increases in HyPer fluorescence were detected after treatment of ≥5 μM, but not after 1 μM H 2 O 2 . In contrast, no changes in HyPer fluorescence were observed after AngII (100 nM) stimulation in control or SOD overexpressing neurons. These data suggest that AngII does not increase H 2 O 2 levels in SOD overexpressing neurons, or does so at concentrations below the level of HyPer detection. These data further support the hypothesis that SOD overexpression inhibits AngII intra‐neuronal signaling by decreasing O 2 •− levels, but not by increasing H 2 O 2 levels. AHA 0930204N.