Báo cáo y học: "The aryl hydrocarbon receptor-mediated disruption of vitellogenin synthesis in the fish liver: Cross-talk between AHR- and ERα-signalling pathway"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Critical Care giúp cho các bạn có thêm kiến thức về ngành y học đề tài: The aryl hydrocarbon receptor-mediated disruption of vitellogenin synthesis in the fish liver: Cross-talk between AHR- and ERα-signalling pathways. | BioMed Central Comparative Hepatology Research Open Access The aryl hydrocarbon receptor-mediated disruption of vitellogenin synthesis in the fish liver Cross-talk between AHR- and ERa-signalling pathways Vahid Bemanian1 2 Rune Male 1 and Anders Goksoyr1 2 Address department of Molecular Biology University of Bergen POBox 7800 N-5020 Bergen Norway and 2Biosense Laboratories AS N-5008 Bergen Norway Email Vahid Bemanian - Rune Male - Anders Goksoyr - anders@ Corresponding author Published 02 May 2004 Received 05 September 2003 Accepted 02 May 2004 Comparative Hepatology 2004 3 2 This article is available from http content 3 1 2 2004 Bemanian et al licensee BioMed Central Ltd. This is an Open Access article verbatim copying and redistribution of this article are permitted in all media for any purpose provided this notice is preserved along with the article s original URL. Abstract Background In the fish liver the synthesis of egg yolk protein precursor vitellogenin VTG is under control of the estrogen receptor alpha ERa . Environmental contaminants such as 2 3 7 8-tetrachloro-dibenzo-p-dioxin TCDD are suspected to have antiestrogenic effects. The aryl hydrocarbon receptor AHR is the initial cellular target for TCDD and related compounds. The AHR is a ligand-activated transcription factor that stimulates the expression of the genes encoding xenobiotic metabolizing enzymes such as cytochrome P450 IA CYPIA . In this study the effects of activation of AHR on the hepatic expression of VTG and ERa genes in primary cultured salmon hepatocytes have been investigated. Results The expression of the genes encoding VTG and ERa were strongly induced by 17P-estradiol E2 . However the expression of VTG was disrupted by exposure of the cells to TCDD while CYPIA expression was enhanced. The effect of TCDD on VTG and CYPIA expression was annulled by the AHR-inhibitor a-naphthoflavone. Furthermore

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