Aquaporin 4 (AQP4) is a predominant water channel protein in mammalian brains, localized in the astrocyte plasma membrane. The regulation of AQP4 is believed to be important for the homeostasis of water in the brain, but the AQP4 regulatory mechanisms are not yet known. In this study, we investigate
Testosterone up-regulates aquaporin-4 expression in cultured astrocytes
✍ Scribed by Feng Gu; Ryuji Hata; Kazuko Toku; Lihua Yang; Yong-Jie Ma; Nobuji Maeda; Masahiro Sakanaka; Junya Tanaka
- Publisher
- John Wiley and Sons
- Year
- 2003
- Tongue
- English
- Weight
- 253 KB
- Volume
- 72
- Category
- Article
- ISSN
- 0360-4012
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✦ Synopsis
Abstract
Aquaporin‐4 (AQP4) is located on astrocyte endfeet that face blood vessels in the brain and in the pia. It is thought to play a crucial role in the development of brain edema. To confirm the notion that sex steroids and dexamethasone influence brain edema through AQP4 regulation, we investigated the effects of 17β‐estradiol, testosterone, and dexamethasone on the expression of AQP4 in cultured astrocytes. Testosterone significantly up‐regulated AQP4 at the level of both protein and mRNA. At a concentration of 100 nM, testosterone significantly increased AQP4 protein levels and ameliorated the osmotic fragility of astrocytes from hypoosmotic stress, suggesting that the increased levels of AQP4 facilitated the testosterone function. Moreover, this effect was attenuated by the protein kinase C activator 12‐O‐tetradecanoylphorbol 13‐acetate, which can rapidly decrease AQP4 mRNA expression, indicating that the response was specific. These results indicate that AQP4 can alter the osmotic fragility of astrocytes and that testosterone can influence brain edema through AQP4 regulation, whereas 17β‐estradiol and dexamethasone cannot. © 2003 Wiley‐Liss, Inc.
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## Abstract Aquaporin‐4 (AQP4), a water channel protein, is abundantly expressed in astrocytes and plays a key role in the development of brain edema. However, it is not clear whether AQP4 contributes to astrocytic swelling in hypoxia–ischemia (HI). To investigate the roles of AQP4 in astrocytic sw