Gene structure and differential modulation of multiple rockbream (Oplegnathus fasciatus) hepcidin isoforms resulting from different biological stimulations

被引:42
作者
Cho, Young S. [1 ]
Lee, Sang Y. [1 ]
Kim, Ki H. [2 ]
Kim, Sung K. [3 ]
Kim, Dong S. [1 ]
Nam, Yoon K. [1 ]
机构
[1] Pukyong Natl Univ, Dept Aquaculture, Pusan 608737, South Korea
[2] Pukyong Natl Univ, Dept Aquat Life Med, Pusan 608737, South Korea
[3] Pukyong Natl Univ, Fac Food Sci & Biotechnol, Pusan 608737, South Korea
关键词
Hepcidin isoforms; Gene expression; Bacterial challenge; Viral infection; Iron overload; Promoter characteristics; Fish innate immunity; Rockbream (Oplegnathus fasciatus); ANTIMICROBIAL PEPTIDE HEPCIDIN; EXPRESSION ANALYSIS; IRON-METABOLISM; BASS HEPCIDIN; SEA BASS; FISH; ORGANIZATION; CLONING; HORMONE;
D O I
10.1016/j.dci.2008.07.009
中图分类号
S9 [水产、渔业];
学科分类号
0908 ;
摘要
Hepcidin, an antimicrobial and iron-regulating peptide, is a key molecule of the innate immune system of bony fish. In this study, four isoforms of hepcidin genes were characterized from a marine Perciform fish, rockbream (Oplegnathus fasciatus), and the transcriptional modulations of these isoforms in response to different biological stimulations were also examined. All rockbream hepcidin isoform genes exhibited a tripartite structure and their promoter regions displayed typical binding motifs for the transcription factors including C/EBP, HNF, AP, NF-k beta, GATA, USF and/or STAT. Hepcidin transcripts in juvenile or fingerling tissues were dramatically induced during experimental challenges with various bacterial species, iron overload and rockbream iridovirus infection. The transcription of hepcidins was regulated in an isoform- and tissue-specific fashion. In addition, we identified for the first time that partially processed hepcidin transcripts were significantly elevated during bacterial infection and iron overload. Results from this study provide a good basis to better understand the isoform-specific role of hepcidin in the fish innate immune system. (C) 2008 Elsevier Ltd. All rights reserved.
引用
收藏
页码:46 / 58
页数:13
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