Ryuichi Katada, Kana Sugimoto, Motonori Yoshida, Hiroshi Matsumoto
{"title":"乙醇增加高钠条件下星形胶质细胞水通道蛋白-4的表达。","authors":"Ryuichi Katada, Kana Sugimoto, Motonori Yoshida, Hiroshi Matsumoto","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>Ethanol increases brain aquaporin-4 (AQP4) expression after traumatic brain injury (TBI), leading to augment mortality and morbidity after TBI. AQP4 is regulated by sodium ion channels/transporters. Ethanol affects the ion channels/transporters. From these findings, we hypothesized that ethanol may have different effects on AQP4 expression in hypo- or hyper-sodium condition. In this study, rat primary astrocytes were incubated in iso-, hypo- or hyper-sodium MEM medium with 10% calf serum. Ethanol was added to each medium simultaneously. And to check whether hypo/hyper-sodium condition could change AQP4 expression after ethanol exposure or not, astrocytes were incubated in iso-sodium with ethanol, followed by changed to hypo/hyper-sodium with the same concentration of ethanol. Astrocyte AQP4 expression was increased in hypo-sodium exposure. Hypo-sodium with ethanol did not change AQP4 expression significantly, on the other hand, hyper-sodium with ethanol decreased AQP4 expression for short time exposure, and increased it for long time exposure. Hyper-sodium changing increased astrocyte AQP4 expression under EtOH exposure. These findings suggest that AQP4 expression is regulated by sodium ion or ion channels/transporters. And ethanol affects sodium ion channels/transporters, which is involved in AQP4 expression under ethanol.</p>","PeriodicalId":79450,"journal":{"name":"Nihon Arukoru Yakubutsu Igakkai zasshi = Japanese journal of alcohol studies & drug dependence","volume":"49 3","pages":"188-94"},"PeriodicalIF":0.0000,"publicationDate":"2014-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Ethanol increases astrocyte aquaporin-4 expression under hyper-sodium condition.\",\"authors\":\"Ryuichi Katada, Kana Sugimoto, Motonori Yoshida, Hiroshi Matsumoto\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Ethanol increases brain aquaporin-4 (AQP4) expression after traumatic brain injury (TBI), leading to augment mortality and morbidity after TBI. AQP4 is regulated by sodium ion channels/transporters. Ethanol affects the ion channels/transporters. From these findings, we hypothesized that ethanol may have different effects on AQP4 expression in hypo- or hyper-sodium condition. In this study, rat primary astrocytes were incubated in iso-, hypo- or hyper-sodium MEM medium with 10% calf serum. Ethanol was added to each medium simultaneously. And to check whether hypo/hyper-sodium condition could change AQP4 expression after ethanol exposure or not, astrocytes were incubated in iso-sodium with ethanol, followed by changed to hypo/hyper-sodium with the same concentration of ethanol. Astrocyte AQP4 expression was increased in hypo-sodium exposure. Hypo-sodium with ethanol did not change AQP4 expression significantly, on the other hand, hyper-sodium with ethanol decreased AQP4 expression for short time exposure, and increased it for long time exposure. Hyper-sodium changing increased astrocyte AQP4 expression under EtOH exposure. These findings suggest that AQP4 expression is regulated by sodium ion or ion channels/transporters. And ethanol affects sodium ion channels/transporters, which is involved in AQP4 expression under ethanol.</p>\",\"PeriodicalId\":79450,\"journal\":{\"name\":\"Nihon Arukoru Yakubutsu Igakkai zasshi = Japanese journal of alcohol studies & drug dependence\",\"volume\":\"49 3\",\"pages\":\"188-94\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2014-06-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Nihon Arukoru Yakubutsu Igakkai zasshi = Japanese journal of alcohol studies & drug dependence\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Nihon Arukoru Yakubutsu Igakkai zasshi = Japanese journal of alcohol studies & drug dependence","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Ethanol increases astrocyte aquaporin-4 expression under hyper-sodium condition.
Ethanol increases brain aquaporin-4 (AQP4) expression after traumatic brain injury (TBI), leading to augment mortality and morbidity after TBI. AQP4 is regulated by sodium ion channels/transporters. Ethanol affects the ion channels/transporters. From these findings, we hypothesized that ethanol may have different effects on AQP4 expression in hypo- or hyper-sodium condition. In this study, rat primary astrocytes were incubated in iso-, hypo- or hyper-sodium MEM medium with 10% calf serum. Ethanol was added to each medium simultaneously. And to check whether hypo/hyper-sodium condition could change AQP4 expression after ethanol exposure or not, astrocytes were incubated in iso-sodium with ethanol, followed by changed to hypo/hyper-sodium with the same concentration of ethanol. Astrocyte AQP4 expression was increased in hypo-sodium exposure. Hypo-sodium with ethanol did not change AQP4 expression significantly, on the other hand, hyper-sodium with ethanol decreased AQP4 expression for short time exposure, and increased it for long time exposure. Hyper-sodium changing increased astrocyte AQP4 expression under EtOH exposure. These findings suggest that AQP4 expression is regulated by sodium ion or ion channels/transporters. And ethanol affects sodium ion channels/transporters, which is involved in AQP4 expression under ethanol.