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Effect of TPA on aquaporin 4 mRNA expression in cultured rat astrocytes

1999; Wiley; Volume: 25; Issue: 3 Linguagem: Inglês

10.1002/(sici)1098-1136(19990201)25

1098-1136

Ken‐ichi Nakahama, Mamoru Nagano, Atsuko Fujioka, Koh Shinoda, Hiroshi Sasaki,

Ion Transport and Channel Regulation

GliaVolume 25, Issue 3 p. 240-246 Original Article Effect of TPA on aquaporin 4 mRNA expression in cultured rat astrocytes Ken-Ichi Nakahama, Corresponding Author Ken-Ichi Nakahama Department of Anatomy, Kinki University School of Medicine, Osakasayama City, Osaka, JapanDepartment of Anatomy, Kinki University School of Medicine, 377-2 Ohno-Higashi, Osakasayama City, Osaka, 589-8511, Japan.Search for more papers by this authorMamoru Nagano, Mamoru Nagano Department of Anatomy, Kinki University School of Medicine, Osakasayama City, Osaka, JapanSearch for more papers by this authorAtsuko Fujioka, Atsuko Fujioka Department of Anatomy, Kinki University School of Medicine, Osakasayama City, Osaka, JapanSearch for more papers by this authorKoh Shinoda, Koh Shinoda Department of Anatomy, Yamaguchi University, School of Medicine, Ube City, Yamaguchi, JapanSearch for more papers by this authorHiroshi Sasaki, Hiroshi Sasaki Department of Anatomy, Kinki University School of Medicine, Osakasayama City, Osaka, JapanSearch for more papers by this author Ken-Ichi Nakahama, Corresponding Author Ken-Ichi Nakahama Department of Anatomy, Kinki University School of Medicine, Osakasayama City, Osaka, JapanDepartment of Anatomy, Kinki University School of Medicine, 377-2 Ohno-Higashi, Osakasayama City, Osaka, 589-8511, Japan.Search for more papers by this authorMamoru Nagano, Mamoru Nagano Department of Anatomy, Kinki University School of Medicine, Osakasayama City, Osaka, JapanSearch for more papers by this authorAtsuko Fujioka, Atsuko Fujioka Department of Anatomy, Kinki University School of Medicine, Osakasayama City, Osaka, JapanSearch for more papers by this authorKoh Shinoda, Koh Shinoda Department of Anatomy, Yamaguchi University, School of Medicine, Ube City, Yamaguchi, JapanSearch for more papers by this authorHiroshi Sasaki, Hiroshi Sasaki Department of Anatomy, Kinki University School of Medicine, Osakasayama City, Osaka, JapanSearch for more papers by this author First published: 27 January 1999 https://doi.org/10.1002/(SICI)1098-1136(19990201)25:3 3.0.CO;2-CCitations: 56AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Abstract 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 investigated the effect of a protein kinase C (PKC) activator on the expression of AQP4 mRNA in cultured rat astrocytes. Cultured rat astrocytes constitutively expressed AQP4 mRNA. Treatment of the cells with 0.1 μM of phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA), an activator of PKC, caused a rapid decrease in AQP4 mRNA. This effect was time- and dose-dependent. The TPA-induced decrease in AQP4 mRNA was inhibited by a relatively specific PKC inhibitor, 1-(5-isoquinoline sulfonyl)-2-methylpiperazine (H7) in a dose-dependent manner. Moreover, prolonged treatment of the cells with TPA eliminated the subsequent decrease in AQP4 mRNA by TPA. These results strongly suggest that the TPA-induced decrease in AQP4 mRNA is mediated by PKC activation. To test whether the effect of TPA requires protein synthesis, astrocytes were pretreated with cycloheximide, an inhibitor of protein synthesis. Pretreatment of the cells with cycloheximide did not inhibit the decrease in AQP4 mRNA induced by TPA. To test whether the TPA-induced decrease in AQP4 was due to a decrease in the mRNA stability, we examined the effect of actinomycin D, an inhibitor of transcription, on TPA-treated cells. The stability of AQP4 mRNA was not decreased by the pretreatment of the cells with actinomycin D. The results suggest that AQP4 mRNA is inhibited by TPA via PKC activation without de novo protein synthesis, and that the inhibition of AQP4 mRNA could be at the transcriptional level. GLIA 25:240–246, 1999. © 1999 Wiley-Liss, Inc. Citing Literature Volume25, Issue31 February 1999Pages 240-246 RelatedInformation