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Aberrant expression of liver microRNA in chickens infected with subgroup J avian leukosis virus

文献类型: 外文期刊

作者: Li, Hongmei 1 ; Ji, Jun 1 ; Xie, Qingmei 1 ; Shang, Huiqin 1 ; Zhang, Huanmin 2 ; Xin, Xuegang 3 ; Chen, Feng 1 ; Sun, Ba 1 ;

作者机构: 1.S China Agr Univ, Coll Anim Sci, Guangzhou 510642, Guangdong, Peoples R China

2.ARS, USDA, Avian Dis & Oncol Lab, E Lansing, MI 48823 USA

3.Guangdong Acad Agr Sci, Inst Anim Sci, State Key Lab Livestock & Poultry Breeding, Guangzhou 510640, Peoples R China

4.Sun Yat Sen Univ, Coll Life Sci, State Key Lab Biocontrol, Guangzhou 510006, Guangdong, Peoples R China

关键词: Chicken;MicroRNA;Subgroup J avian leukosis virus

期刊名称:VIRUS RESEARCH ( 影响因子:3.303; 五年影响因子:3.445 )

ISSN:

年卷期:

页码:

收录情况: SCI

摘要: Subgroup J avian leukosis virus (ALV-J) is an oncogenic retrovirus primarily causing myeloid leukosis (ML) in broilers. Although ALV is well under control in a few countries including the USA, poultry industry in many parts of the world continues suffering from serious economic loss due to sporadic or widespread ALV infection, especially ALV-J infection. ALV-J infection of chickens is reportedly mediated by a cellular receptor. So far, however, no genetic variant of the receptor gene that confers resistance to ALV-J has been identified. To advance our understanding on epigenetic factors that are involved in the event of ALV-J infection, we examined the expression of miRNAs in livers of 10-week-old chickens uninfected or infected with ALV-J by miRNA microarray analysis. Our data showed there were 12 miRNAs differentially expressed in liver between the uninfected and infected groups (P< 0.01). Of which, the expressions of seven miRNAs (gga-mir-221, gga-mir-222, gga-mir-1456, gga-mir-1704, gga-mir-1777, gga-mir-1790, and gga-mir-2127,) were upregulated by ALV-J infection and may be involved in oncogenicity. The other five miRNAs (gga-let-7b, gga-let-7i, gga-mir-125b, gga-mir-375, and gga-mir-458) were significantly downregulated. The downregulated miRNAs may play important roles in tumor suppression. This finding paves the way for further exploration of epigenetic influence on tumorigenicity upon ALV-J infection.

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