Subgroup J avian leukosis virus infection of chicken dendritic cells induces apoptosis via the aberrant expression of microRNAs

Liu, Di; Dai, Manman; Xu, Zhengping; Cao, Weijun; Liao, Ming

doi:10.1038/srep20188

Cited by 29 publications

(32 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Accumulating evidences demonstrated that lncRNA growth arrest-specific 5 (GAS5) acted as a powerful regulator of various biological activities, including tumor metastasis [29], vascular remodeling [30], autoimmune and inflammatory diseases [31]. Recently, GAS5 has been reported to involve in autophagy in NSCLC cells [32], and negatively correlated with mTOR [33,34], which is a crucial regulator of autophagy [35]. Although GAS5 has been suggested to mediate autophagy program, the underlying mechanism still remains to be further confirmed.…”

Section: Introductionmentioning

confidence: 99%

Knockdown of Long Non-Coding RNA GAS5 Increases miR-23a by Targeting ATG3 Involved in Autophagy and Cell Viability

Huang

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: Autophagy is a process of evolutionarily conservative degradation, which could maintain cellular homeostasis and cope with various types of stress. LncRNAs are considered as competing endogenous RNAs (ceRNAs) contributing to autophagy. GAS5 has been suggested as a new potential factor to mediate autophagy pathway and the underlying mechanism remains to be further confirmed. This study was taken to identify the effect of GAS5/miR-23a/ATG3 axis on autophagy and cell viability. Methods: The western blotting assay was used to detecte the protein levels of LC3, mTOR, Beclin-1, ATG3, ATG5-ATG12 complex and p62. The mRNA level of Pre-miR-23a, Pri-miR-23a, miR-23a, GAS5, LC3, mTOR and ATG3 were quantified by real-time RT-PCR. Dual-luciferase reporter assays were performed to confirm the direct binding of miR-23a and ATG3 or GAS5. Cell viability was evaluated by CCK-8 and flow cytometry. Results: We showed that miR-23a could directly suppress ATG3 expression in 293T cells, which suggested that ATG3 was identified as a target of miR-23a. MiR-23a mimics could restrain LC3 II, Beclin1 levles and ATG5-ATG12 complex formation. Meanwhile, miR-23a also increased the expression of mTOR and p62. Notably, there was a putative miR-23a-binding site in GAS5. MiR-23a overexpression might suppress the GAS5 expression, but the repressive effect was abolished by mutation of binding sites. Importantly, overexpression of GAS5 could inhibit the mature miR-23a and has no effect on miR-23a precursors. Knockdown of GAS5 suppressed the expression of LC3 II, ATG3 and ATG5-ATG12 complex formation, whereas p62 and mTOR levels were promoted. The further results showed that miR-23a overexpression and GAS5 inhibition both significantly suppressed cell viability and promoted the apoptosis rate following LPS stimulation, and knockdown of miR-23a exhibited the opposite effects. Conclusions: Our study revealed that down-regulation GAS5 attenuated cell viability and inhibited autophagy through ATG3-dependent autophagy by regulating miR-23a expression. The results suggested that GAS5/miR-23a/ATG3 axis might be a novel regulatory network contributing to a better understanding of regulation on autophagy program and cell viability.

show abstract

Section: Introductionmentioning

confidence: 99%

Knockdown of Long Non-Coding RNA GAS5 Increases miR-23a by Targeting ATG3 Involved in Autophagy and Cell Viability

Huang

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

show abstract

“…From 2002 to 2010, ALV-J infection became a common infectious disease in China’s poultry industry [21]. Because of recent worldwide eradication efforts, ALV-J infection now rarely occurs in white-feather broilers, but has gradually returned to local chicken farms in China [22].…”

Section: Discussionmentioning

confidence: 99%

Seroprevalence of avian hepatitis E virus and avian leucosis virus subgroup J in chicken flocks with hepatitis syndrome, China

Sun

Liu

et al. 2016

BMC Vet Res

View full text Add to dashboard Cite

BackgroundFrom 2014 to 2015 in China, many broiler breeder and layer hen flocks exhibited a decrease in egg production and some chickens developed hepatitis syndrome including hepatomegaly, hepatic necrosis and hemorrhage. Avian hepatitis E virus (HEV) and avian leucosis virus subgroup J (ALV-J) both cause decreasing in egg production, hepatomegaly and hepatic hemorrhage in broiler breeder and layer hens. In the study, the seroprevalence of avian HEV and ALV-J in these flocks emerging the disease from Shandong and Shaanxi provinces were investigated.ResultsA total of 1995 serum samples were collected from 14 flocks with hepatitis syndrome in Shandong and Shaanxi provinces, China. Antibodies against avian HEV and ALV-J in these serum samples were detected using iELISAs. The seroprevalence of anti-avian HEV antibodies (35.09%) was significantly higher than that of anti-ALV-J antibodies (2.16%) (p = 0.00). Moreover, the 43 serum samples positive for anti-ALV-J antibodies were all also positive for anti-avian HEV antibodies. In a comparison of both provinces, Shandong chickens exhibited a significantly higher seroprevalence of anti-avian HEV antibodies (42.16%) than Shaanxi chickens (26%) (p = 0.00). In addition, the detection of avian HEV RNA and ALV-J cDNA in the liver samples from the flocks of two provinces also showed the same results of the seroprevalence.ConclusionsIn the present study, the results showed that avian HEV infection is widely prevalent and ALV-J infection is endemic in the flocks with hepatitis syndrome from Shandong and Shaanxi provinces of China. These results suggested that avian HEV infection may be the major cause of increased egg drop and hepatitis syndrome observed during the last 2 years in China. These results should be useful to guide development of prevention and control measures to control the diseases within chicken flocks in China.Electronic supplementary materialThe online version of this article (doi:10.1186/s12917-016-0892-4) contains supplementary material, which is available to authorized users.

show abstract

“…An ex vivo study demonstrated that ALV-J could infect bone marrow-derived DCs (BM-DCs) during the early stages of differentiation and trigger apoptosis (44). Further studies showed that ALV-J inhibits the differentiation and maturation of BM-DCs and alters cytokine expression, causing aberrant antigen presentation and an altered immune response (19).…”

Section: Immunity Against Alvmentioning

confidence: 99%

“…Chicken macrophages and DCs can be directly infected by ALV and induce innate immunity (40, 44). However, we still have no clear knowledge of the regulation of the global innate immune response to ALV infection and ALV evasion of the host innate immune response.…”

Section: Immunity Against Alvmentioning

confidence: 99%

Immunity to Avian Leukosis Virus: Where Are We Now and What Should We Do?

Feng

Zhang

2016

Front. Immunol.

View full text Add to dashboard Cite

Avian leukosis virus (ALV) is an avian oncogenic retrovirus causing enormous economic losses in the global poultry industry. Although ALV-related research has lasted for more than a century, there are no vaccines to protect chickens from ALV infection. The interaction between chickens and ALV remains not fully understood especially with regard to the host immunity. The current review provides an overview of our current knowledge of innate and adaptive immunity induced by ALV infection. More importantly, we have pointed out the unknown area involved in ALV-related studies, which is worthy of our serious exploring in future.

show abstract

Subgroup J avian leukosis virus infection of chicken dendritic cells induces apoptosis via the aberrant expression of microRNAs

Cited by 29 publications

References 42 publications

Knockdown of Long Non-Coding RNA GAS5 Increases miR-23a by Targeting ATG3 Involved in Autophagy and Cell Viability

Knockdown of Long Non-Coding RNA GAS5 Increases miR-23a by Targeting ATG3 Involved in Autophagy and Cell Viability

Seroprevalence of avian hepatitis E virus and avian leucosis virus subgroup J in chicken flocks with hepatitis syndrome, China

Immunity to Avian Leukosis Virus: Where Are We Now and What Should We Do?

Contact Info

Product

Resources

About