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Asian-Australas J Anim Sci > Accepted Articles
DOI: https://doi.org/10.5713/ajas.19.0874    [Accepted] Published online February 25, 2020.
Effect of JAK-STAT pathway in regulation of fatty liver hemorrhagic syndrome in chickens
Yaling Zhu2,3  , Huirong Mao1  , Gang Peng1  , Qingjie Zeng1  , Jiming Ruan1,*  , Jianzhen Huang1,* 
1College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang 330045, China
2Department of Pathophysiology, Anhui Medical University, Hefei 230000, China
3Laboratory Animal Research Center, College of Basic Medical Science, Anhui Medical University, Hefei 230000, China
Correspondence:  Jiming Ruan,Email: rjm903@163.com
Jianzhen Huang, Tel: +86-791-83813080, Fax: +86-791-83900189, Email: hjzh0722@aliyun.com
Received: 12 November 2019   • Revised: 13 January 2020   • Accepted: 10 February 2020
To explore the molecular mechanisms of fatty liver hemorrhagic syndrome (FLHS) in laying hens, an experiment was conducted to reveal the differences in histopathological observation and gene expression between FLHS group and normal group.
We compared the histopathological difference using hematoxylin and eosin staining and proceeded with RNA sequencing of adipose tissue to search differentially expressed genes and enriched biological processes and pathways. Then we validated the mRNA expression levels by real-time PCR and quantified protein levels in the circulation by enzyme-linked immunosorbent assay (ELISA).
100 differentially expressed transcripts corresponding to 66 genes (DEGs) were identified between FLHS-affected group and normal group. Seven DEGs were significantly enriched in the immune response process and lipid metabolic process, including PLA2G5, WFIKKN2, DEGS2, PLIN3, IL6, CNTF and SOCS3. And these genes could be the targets of immune response and be involved in metabolic homeostasis during the process of FLHS in laying hens. Based on functional categories of the DEGs, we further proposed a model to explain the etiology and pathogenesis of FLHS. IL6 and SOCS3 mediate inflammatory responses and the satiety hormone of leptin, induce dysfunction of Jak-STAT signaling pathway, leading to insulin resistance and lipid metabolic disorders. Conversely, CNTF may reduce tissue destruction during inflammatory attacks and confer protection from inflammation-induced insulin resistance in FLHS chickens.
These findings highlight the therapeutic implications of targeting the JAK-STAT pathway. Inhibition of IL6 and SOCS3 and facilitation of CNTF could serve as a favorable strategy to enhance insulin action and improve glucose homoeostasis, which are of importance for treating obesity-related disorders for chickens.
Keywords: Fatty Liver Hemorrhagic Syndrome; RNA-Seq; JAK-STAT Pathway; Differentially Expressed Genes; Chicken
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