Involvement of fish signal transducer and activator of transcription 3 (STAT3) in nodavirus infection induced cell death

Huang, Youhua; Huang, Xiaohong; Yang, Ying; Wang, Wei; Yu, Yang; Qin, Qiwei

doi:10.1016/j.fsi.2014.12.031

Cited by 32 publications

(9 citation statements)

References 56 publications

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“…In contrast, STAT3 is a crucial transcription factor for M2 macrophage polarization (60). STAT1 and STAT3 are also implicated in the immune response in teleost fish (61,62). In this study, we found that STAT1 and STAT3 were activated in CXCR3.1 + and CXCR3.2 + macrophages, respectively, after E. coli treatment.…”

Section: Discussionmentioning

confidence: 49%

CXCR3.1 and CXCR3.2 Differentially Contribute to Macrophage Polarization in Teleost Fish

Chen

Rong

et al. 2017

The Journal of Immunology

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The study of multiple copies of chemokine receptor genes in various teleosts has long appealed to investigators seeking to understand the evolution of the immune system. The CXCR CXCR3 gene has two isoforms, CXCR3.1 and CXCR3.2, which are both expressed in macrophages. The distinct roles of teleost CXCR3s have not been identified previously. In this article, we found that CXCR3.1 and CXCR3.2 differentially contributed to macrophage polarization in the teleosts: ayu (), grass carp (), and spotted green pufferfish (). In ayu macrophages, the CXCR3.1 (PaCXCR3.1) gene was constitutively expressed, whereas the CXCR3.2 (PaCXCR3.2) gene was induced postinfection with Upon infection, PaCXCR3.1 and PaCXCR3.2 macrophages showed an M1 and an M2 phenotype, respectively. CXCL9-11-like proteins mediated M1 and M2 polarization by interacting with the PaCXCR3.1 and PaCXCR3.2 proteins on macrophages, respectively. The transcription factors STAT1 and STAT3 were activated in PaCXCR3.1 and PaCXCR3.2 macrophages, respectively. Furthermore, the prognosis of septic ayu adoptively transferred with PaCXCR3.2 macrophages was improved. Our data reveal a previously unknown mechanism for macrophage polarization, suggesting that redundant genes may regulate crucial functions in the teleost immune system.

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Section: Discussionmentioning

confidence: 49%

CXCR3.1 and CXCR3.2 Differentially Contribute to Macrophage Polarization in Teleost Fish

Chen

Rong

et al. 2017

The Journal of Immunology

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“…When autophagy occurs, LC3 becomes conjugated to phosphatidylethanolamine at autophagosome-forming sites, and redistributes from a diffuse pattern to a punctate cytoplasmic pattern (Kabeya et al, 2000;Tanida et al, 2008). Given that our previous studies indicated that RGNNV infection could induce autophagy (Huang et al, 2015), we raised the question of whether autophagy was involved in lysosomal vacuolization during RGNNV infection. To address this issue, we first examined whether autophagosome-like vesicles and the altered distribution for LC3 proteins occurred in vacuolization.…”

Section: Discussionmentioning

confidence: 98%

“…The effects of 3-MA on RGNNV-induced autophagy was determined using a Cyto-ID Autophagy detection kit (Enzo life sciences) as described previously (Huang et al, 2015). Briefly, the cells were seeded into 24-well plates at ∼80% confluence.…”

Section: Evaluation Of Autophagymentioning

confidence: 99%

Autophagy Participates in Lysosomal Vacuolation-Mediated Cell Death in RGNNV-Infected Cells

Huang

Liu

et al. 2020

Front. Microbiol.

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Nervous necrosis virus (NNV) is the etiological agent of viral nervous necrosis (VNN), also known as viral encephalopathy and retinopathy (VER), which results in heavy economic losses to the aquaculture industry worldwide. Dramatic cytoplasmic vacuoles were observed during NNV infection both in vitro and in vivo; however, the origin and mechanism of cytoplasmic vacuolization remains unknown. In this report, we found that the cytoplasmic vacuole morphology became fused and enlarged during infection with red spotted grouper nervous necrosis virus (RGNNV), which was accompanied by increased cell death. Notably, Lyso-Tracker, but not Mito-Tracker or ER-Tracker, was accumulated in the vacuoles, and abnormal lysosome swelling was observed in RGNNV-infected cells, suggesting that the cytoplasmic vacuoles originated from lysosomal organelles. Cytoplasmic vacuolization and cell death in RGNNV-infected cells was completely blocked by the vacuolar H +-ATPase inhibitor (bafilomycin A1), and was significantly weakened by chloroquine (CQ), a lysosomotropic agent that induces the acidification of the lysosomes. This suggests that lysosome acidification was essential for vacuole formation. Significant inhibitory effects on vacuolization and cell death were also observed in the RGNNV-infected cells following treatment with nigericin and monensin (ionophores that uncouple the proton gradient present in lysosomes). This indicated that lysosome function was tightly associated with RGNNV infection-induced cell death. In addition, vacuoles were found to be partially co-localized with GFP-LC3II punctate dots during RGNNV infection. Moreover, the severity of vacuolization and cell death were both significantly decreased after treatment with the autophagy inhibitor, 3-MA, suggesting that autophagy was involved in lysosomal vacuolization and cell death evoked by RGNNV infection. Thus, our results demonstrate that autophagy participates in lysosomal vacuolation-mediated cell death during RGNNV infection, and provides new insight into our understanding of the potential mechanisms underlying nodavirus pathogenesis in vitro.

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“…Interestingly, recent studies revealed that the dual role of STATs as signaling molecules and transcription factors is reflected in autophagy regulation [174][175][176][177][178][179][180][181]. When STATs are not phosphorylated and stay in the cytoplasm, they interact with many autophagyrelated components to regulate the autophagic flux [174][175][176]. STAT1 was reported to affect the function of mTOR, PI3KCIII, ATG7, LC3, Bcl-2, ATG4, and so on [176].…”

Section: Other Important Transcription Factors Of Autophagy Regulatiomentioning

confidence: 99%

“…STAT1 was reported to affect the function of mTOR, PI3KCIII, ATG7, LC3, Bcl-2, ATG4, and so on [176]. STAT3 was also found to interact with mTOR, MAPK, Bcl-2, ULK2, LC3-II, ATG7, ATG5, ATG12, and so on [175]. All of these regulatory proteins play irreplaceable roles at each stage of the formation of autophagy.…”

Section: Other Important Transcription Factors Of Autophagy Regulatiomentioning

confidence: 99%

The update on transcriptional regulation of autophagy in normal and pathologic cells: A novel therapeutic target

Zhang

Guo

Zhao

et al. 2015

Biomedicine & Pharmacotherapy

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Involvement of fish signal transducer and activator of transcription 3 (STAT3) in nodavirus infection induced cell death

Cited by 32 publications

References 56 publications

CXCR3.1 and CXCR3.2 Differentially Contribute to Macrophage Polarization in Teleost Fish

CXCR3.1 and CXCR3.2 Differentially Contribute to Macrophage Polarization in Teleost Fish

Autophagy Participates in Lysosomal Vacuolation-Mediated Cell Death in RGNNV-Infected Cells

The update on transcriptional regulation of autophagy in normal and pathologic cells: A novel therapeutic target

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