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Cgi-miR-92d indirectly regulates TNF expression by targeting CDS region of lipopolysaccharide-induced TNF-alpha factor 3 (CgLITAF3) in oyster Crassostrea gigas
Chen, Hao1,3; Jiang, Shuai1; Wang, Lin1,3; Wang, Lingling2; Wang, Hao1; Qiu, Limei1; Song, Linsheng2
2016-08-01
发表期刊FISH & SHELLFISH IMMUNOLOGY
卷号55页码:577-584
文章类型Article
摘要Tumor necrosis factor alpha (TNF-alpha) mediated inflammatory response plays indispensable roles in organisms defending against the invaded bacteria, during which microRNAs have been found crucial by controlling multiple TNF-alpha-related genes. In the present study, cgi-miR-92d was annotated as a member of miR-17-92 family and could target the CDS region of lipopolysaccharide (LPS)-induced TNF-alpha factor (CgLITAF3) in oyster Crassostrea gigas. It was observed that cgi-miR-92d could be vigorously modulated by Vibrio splendidus or LPS stimulation while CgLITAF3 altered oppositely. Two putative binding sites of cgi-miR-92d were then found at CDS region of CgLITAF3. The interaction between cgi-miR-92d and CgLITAF3 was subsequently verified both in vitro and in vivo. As a result, a significant decrease of cellular luminescence was observed in CgLITAF3 luciferase reporter assay when cgi-miR-92d was overexpressed. The luminescent decrease was then recuperated when cgi-miR-92d inhibitor was co-transfected with miRNA mimics. Besides, CgLITAF3 transcripts were significantly down-regulated when cgi-miR-92d was overexpressed in vivo during V. splendidus challenge. Gain-of-function assay of CgLITAF3 was then conducted in HEK293T cells to verify its function. Consequently, a significant increase of TNF-alpha was observed during the assay. At the meantime, CgTNF was also down-regulated in gain-of-function assay of cgi-miR-92 in vivo, which was a member of TNF superfamily in oysters which could be robustly induced after pathogen stimulation. Together, these results verify the interaction between CgLITAF3 and cgi-miR-92d, which might dedicate crucially in the repaid activation of CgTNF expression during inflammatory response of oysters. (C) 2016 Elsevier Ltd. All rights reserved.
关键词Oyster Immunomodulation Mir-17-92 Family Tumor Necrosis Factor Lps-induced Tnf-alpha Factor Inflammation
DOI10.1016/j.fsi.2016.06.036
收录类别SCI
语种英语
WOS记录号WOS:000381537000063
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文献类型期刊论文
版本出版稿
条目标识符http://ir.qdio.ac.cn/handle/337002/135864
专题实验海洋生物学重点实验室
作者单位1.Chinese Acad Sci, Inst Oceanol, Key Lab Expt Marine Biol, Qingdao 266071, Peoples R China
2.Dalian Ocean Univ, Key Lab Mariculture & Stock Enhancement North Chi, Minist Agr, Dalian 116023, Peoples R China
3.Univ Chinese Acad Sci, Beijing 100049, Peoples R China
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Chen, Hao,Jiang, Shuai,Wang, Lin,et al. Cgi-miR-92d indirectly regulates TNF expression by targeting CDS region of lipopolysaccharide-induced TNF-alpha factor 3 (CgLITAF3) in oyster Crassostrea gigas[J]. FISH & SHELLFISH IMMUNOLOGY,2016,55:577-584.
APA Chen, Hao.,Jiang, Shuai.,Wang, Lin.,Wang, Lingling.,Wang, Hao.,...&Song, Linsheng.(2016).Cgi-miR-92d indirectly regulates TNF expression by targeting CDS region of lipopolysaccharide-induced TNF-alpha factor 3 (CgLITAF3) in oyster Crassostrea gigas.FISH & SHELLFISH IMMUNOLOGY,55,577-584.
MLA Chen, Hao,et al."Cgi-miR-92d indirectly regulates TNF expression by targeting CDS region of lipopolysaccharide-induced TNF-alpha factor 3 (CgLITAF3) in oyster Crassostrea gigas".FISH & SHELLFISH IMMUNOLOGY 55(2016):577-584.
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