Effect of JAK-STAT pathway in regulation of fatty liver hemorrhagic syndrome in chickens
Objective 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. Methods We compared the histopathological differenc...
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| Format: | Article |
| Language: | English |
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Asian-Australasian Association of Animal Production Societies
2021-01-01
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| Series: | Animal Bioscience |
| Subjects: | |
| Online Access: | http://www.animbiosci.org/upload/pdf/ajas-19-0874.pdf |
| _version_ | 1819120631437852672 |
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| author | Yaling Zhu Huirong Mao Gang Peng Qingjie Zeng Qing Wei Jiming Ruan Jianzhen Huang |
| author_facet | Yaling Zhu Huirong Mao Gang Peng Qingjie Zeng Qing Wei Jiming Ruan Jianzhen Huang |
| author_sort | Yaling Zhu |
| collection | DOAJ |
| description | Objective 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. Methods 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 polymerase chain reaction and quantified protein levels in the circulation by enzyme-linked immunosorbent assay. Results We identified 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 phospholipase A2 group V, WAP kunitz and netrin domain containing 2, delta 4-desaturase sphingolipid 2, perilipin 3, interleukin-6 (IL-6), ciliary neurotrophic factor (CNTF), and suppressor of cytokine signaling 3 (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. IL-6 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. Conclusion 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. |
| first_indexed | 2024-12-22T06:23:44Z |
| format | Article |
| id | doaj.art-fc3a4d26846b4e5bbe8d2c51773b23b0 |
| institution | Directory Open Access Journal |
| issn | 2765-0189 2765-0235 |
| language | English |
| last_indexed | 2024-12-22T06:23:44Z |
| publishDate | 2021-01-01 |
| publisher | Asian-Australasian Association of Animal Production Societies |
| record_format | Article |
| series | Animal Bioscience |
| spelling | doaj.art-fc3a4d26846b4e5bbe8d2c51773b23b02022-12-21T18:35:54ZengAsian-Australasian Association of Animal Production SocietiesAnimal Bioscience2765-01892765-02352021-01-0134114315310.5713/ajas.19.087424480Effect of JAK-STAT pathway in regulation of fatty liver hemorrhagic syndrome in chickensYaling Zhu0Huirong Mao1Gang Peng2Qingjie Zeng3Qing Wei4Jiming Ruan5Jianzhen Huang6 College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang, 330045, China College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang, 330045, China College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang, 330045, China College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang, 330045, China College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang, 330045, China College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang, 330045, China College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang, 330045, ChinaObjective 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. Methods 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 polymerase chain reaction and quantified protein levels in the circulation by enzyme-linked immunosorbent assay. Results We identified 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 phospholipase A2 group V, WAP kunitz and netrin domain containing 2, delta 4-desaturase sphingolipid 2, perilipin 3, interleukin-6 (IL-6), ciliary neurotrophic factor (CNTF), and suppressor of cytokine signaling 3 (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. IL-6 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. Conclusion 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.http://www.animbiosci.org/upload/pdf/ajas-19-0874.pdffatty liver hemorrhagic syndromerna-seqjak-stat pathwaydifferentially expressed geneschicken |
| spellingShingle | Yaling Zhu Huirong Mao Gang Peng Qingjie Zeng Qing Wei Jiming Ruan Jianzhen Huang Effect of JAK-STAT pathway in regulation of fatty liver hemorrhagic syndrome in chickens Animal Bioscience fatty liver hemorrhagic syndrome rna-seq jak-stat pathway differentially expressed genes chicken |
| title | Effect of JAK-STAT pathway in regulation of fatty liver hemorrhagic syndrome in chickens |
| title_full | Effect of JAK-STAT pathway in regulation of fatty liver hemorrhagic syndrome in chickens |
| title_fullStr | Effect of JAK-STAT pathway in regulation of fatty liver hemorrhagic syndrome in chickens |
| title_full_unstemmed | Effect of JAK-STAT pathway in regulation of fatty liver hemorrhagic syndrome in chickens |
| title_short | Effect of JAK-STAT pathway in regulation of fatty liver hemorrhagic syndrome in chickens |
| title_sort | effect of jak stat pathway in regulation of fatty liver hemorrhagic syndrome in chickens |
| topic | fatty liver hemorrhagic syndrome rna-seq jak-stat pathway differentially expressed genes chicken |
| url | http://www.animbiosci.org/upload/pdf/ajas-19-0874.pdf |
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