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Contradictory effects of superoxide and hydrogen peroxide on K Ca3.1 in human endothelial cells

Title
Contradictory effects of superoxide and hydrogen peroxide on K Ca3.1 in human endothelial cells
Authors
Choi S.Na H.-Y.Kim J.A.Cho S.-E.Suh S.H.
Ewha Authors
서석효최신규
SCOPUS Author ID
서석효scopus; 최신규scopus
Issue Date
2013
Journal Title
Korean Journal of Physiology and Pharmacology
ISSN
1226-4512JCR Link
Citation
vol. 17, no. 3, pp. 181 - 187
Indexed
SCIE; SCOPUS; KCI WOS scopus
Abstract
Reactive oxygen species (ROS) are generated in various cells, including vascular smooth muscle and endothelial cells, and regulate ion channel functions. KCa3.1 plays an important role in endothelial functions. However, the effects of superoxide and hydrogen peroxide radicals on the expression of this ion channel in the endothelium remain unclear. In this study, we examined the effects of ROS donors on KCa3.1 expression and the K+ current in primary cultured human umbilical vein endothelial cells (HUVECs). The hydrogen peroxide donor, tert-butyl hydroperoxide (TBHP), upregulated KCa3.1 expression, while the superoxide donors, xanthine/xanthine oxidase mixture (X/XO) and lysophosphatidylcholine (LPC), downregulated its expression, in a concentration-dependent manner. These ROS donor effects were prevented by antioxidants or superoxide dismustase. Phosphorylated extracellular signal-regulated kinase (pERK) was upregulated by TBHP and downregulated by X/XO. In addition, repressor element-1-silencing transcription factor (REST) was downregulated by TBHP, and upregulated by X/XO. Furthermore, KCa3.1 current, which was activated by clamping cells with 1 μM Ca2+ and applying the KCa3.1 activator 1-ethyl-2-benzimidazolinone, was further augmented by TBHP, and inhibited by X/XO. These effects were prevented by antioxidants. The results suggest that hydrogen peroxide increases KCa3.1 expression by upregulating pERK and downregulating REST, and augments the K+ current. On the other hand, superoxide reduces KCa3.1 expression by downregulating pERK and upregulating REST, and inhibits the K+ current. ROS thereby play a key role in both physiological and pathological processes in endothelial cells by regulating KCa3.1 and endothelial function.
DOI
10.4196/kjpp.2013.17.3.181
Appears in Collections:
의과대학 > 의학과 > Journal papers
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