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Contradictory Effects of Superoxide and Hydrogen Peroxide on KCa3.1 in Human Endothelial Cells

Authors
 Shinkyu Choi  ;  Hye-Young Na, Ji Aee Kim, Sung-Eun Cho  ;  Suk Hyo Suh 
Citation
 KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY, Vol.17(3) : 181-187, 2013 
Journal Title
 KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY 
ISSN
 1226-4512 
Issue Date
2013
Keywords
Ca2+-activated K+ channel ; Endothelial cells ; Hydrogen peroxide ; Superoxide
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 lysopho-sphatidylcholine (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 Ca(2+) 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.
Files in This Item:
T201306330.pdf Download
DOI
10.4196/kjpp.2013.17.3.181
Appears in Collections:
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers
Yonsei Authors
Na, Hye Young(나혜영) ORCID logo https://orcid.org/0000-0002-2886-9926
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/158535
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