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Altered Redox State Modulates Endothelial K(Ca)2.3 and K(Ca)3.1 Levels in Normal Pregnancy and Preeclampsia

Title
Altered Redox State Modulates Endothelial K(Ca)2.3 and K(Ca)3.1 Levels in Normal Pregnancy and Preeclampsia
Authors
Choi, ShinkyuKim, Ji AeeLi, Hai-yanLee, Sae-JinSeok, Ye SeonKim, Tae HunHan, Ki-HwanPark, Mi HyeCho, Geum JoonSuh, Suk Hyo
Ewha Authors
서석효박미혜김태헌한기환최선영
SCOPUS Author ID
서석효scopus; 박미혜scopus; 김태헌scopus; 한기환scopus; 최선영scopus
Issue Date
2019
Journal Title
ANTIOXIDANTS & REDOX SIGNALING
ISSN
1523-0864JCR Link

1557-7716JCR Link
Citation
ANTIOXIDANTS & REDOX SIGNALING vol. 30, no. 4, pp. 505 - 519
Keywords
pregnancypreeclampsiaCa2+-activated K+ channelsendothelial cellsredox state
Publisher
MARY ANN LIEBERT, INC
Indexed
SCI; SCIE; SCOPUS WOS scopus
Document Type
Article
Abstract
Aims: Altered redox state has been related to the development of normal pregnancy (NP) and preeclampsia (PE). Endothelial K(Ca)2.3 and K(Ca)3.1 (K(Ca)s) play an important role in vasodilation, and K(Ca)s levels are affected by oxidative stress. We investigated the mechanisms of oxidative stress-mediated K(Ca)s expression modulation during NP and PE. Results: Human uterine microvascular endothelial cells were incubated in serum from normal nonpregnant women (n=13) and women with NP (n=24) or PE (n=15), or in vascular endothelial growth factor (VEGF), oxidized low-density lipoprotein (ox-LDL), progesterone, or estradiol-17 beta (E-2)-containing medium for 24h. NP serum elevated H2O2 levels via reducing catalase and glutathione peroxidase 1 levels, thereby enhancing K(Ca)s levels via a H2O2/fyn/extracellular signal-regulated kinase (ERK)-mediated pathway. VEGF enhanced H2O2 and K(Ca)s levels and K(Ca)3.1 currents. K(Ca)s were upregulated and K(Ca)s activation-induced endothelium-dependent relaxation (EDR) was augmented in vessels from pregnant mice and rats. Whereas PE serum, ox-LDL, progesterone, or soluble fms-like tyrosine kinase 1 (sFlt-1) elevated superoxide levels via elevating NADPH oxidase 2 (NOX2) and NOX4 levels and reducing superoxide dismutase (SOD) 1 levels, thereby downregulating K(Ca)s. sFlt-1 inhibited EDR. PE serum- or progesterone-induced alterations in levels of K(Ca)s were reversed by polyethylene glycol-SOD, NOX inhibition, or E-2. Innovation and Conclusions: This is the first study of how endothelial K(Ca)s levels are modulated during NP and PE. K(Ca)s were upregulated by soluble serum factors such as VEGF via H2O2 generation in NP, and were downregulated by serum factors such as progesterone and ox-LDL via superoxide generation in PE, which may contribute to hemodynamic adaptations in NP or to the development of PE.
DOI
10.1089/ars.2017.7038
Appears in Collections:
의과대학 > 의학과 > Journal papers
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