Astrocytic AEG-1 regulates expression of TREK-1 under acute hypoxia
- Authors
- Kim, Ajung; Jung, Hyun-Gug; Kim, Seung-Chan; Choi, Minji; Park, Jae-Yong; Lee, Seok-Geun; Hwang, Eun Mi
- Issue Date
- 3월-2020
- Publisher
- WILEY
- Keywords
- AEG-1; astrocyte; Hif1 alpha; hypoxia; TREK-1
- Citation
- CELL BIOCHEMISTRY AND FUNCTION, v.38, no.2, pp.167 - 175
- Indexed
- SCIE
SCOPUS
- Journal Title
- CELL BIOCHEMISTRY AND FUNCTION
- Volume
- 38
- Number
- 2
- Start Page
- 167
- End Page
- 175
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/57494
- DOI
- 10.1002/cbf.3469
- ISSN
- 0263-6484
- Abstract
- TREK-1 (TWIK-related K+ channel), a member of the two-pore domain K+ (K2P) channel family, is highly expressed in astrocytes, where it plays a key role in glutamate release and passive conductance. In addition, TREK-1 is induced to protect neurons under pathological conditions such as hypoxia. However, the upstream regulation of TREK-1 remains poorly understood. In this study, we found that AEG-1 (astrocyte elevated gene-1) regulates the expression of astrocytic TREK-1 under hypoxic conditions. Upregulation of AEG-1 increased expression of TREK-1 in astrocytes, and knockdown of AEG-1 dramatically decreased the mRNA and protein levels of TREK-1, which were restored by expression of shRNA-insensitive AEG-1. In addition, expression of TREK-1 was not regulated in the absence of AEG-1, even when HIF1 alpha was present. Together, these results suggest that AEG-1 acts as a major upstream regulator of TREK-1 channels in astrocytes under hypoxia. Significance of the study Previous studies have reported that hypoxia increases the expression of astrocytic TREK-1 and that increased TREK-1 expression protects neuronal cells from apoptosis. However, its cellular mechanism is not clear. In this study we first showed that AEG-1 is a major mediator of hypoxic-regulated TREK-1 expression in normal astrocytes independently of HIF-1 alpha.
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