The activation of p38MAPK and JNK pathways in bovine herpesvirus 1 infected MDBK cells

Zhu, Liqian; Yuan, Chen; Huang, Liyuan; Ding, Xuezhi; Wang, Qianqian; Zhang, Dong; Zhu, Guoqiang

doi:10.1186/s13567-016-0377-2

Cited by 14 publications

(15 citation statements)

References 38 publications

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“…However, the effects of EGFR on BoHV-1 infection are currently unknown. Given that the canonical EGFR downstream effects including PLC-γ1, MAPK, Akt and JNK are unanimously activated during BoHV-1 productive infection in MDBK cells [19,20], we hypothesized that BoHV-1 infection activates EGFR signaling to facilitate viral replication. Furthermore, it has been reported that EGFR is activated in response to radiation-induced DNA damage to promote cell survival [21], and in BoHV-1-infected A549 cells, detectable DNA damage is induced at 24 and 48 hours (h) after infection [22].…”

Section: Introductionmentioning

confidence: 99%

The Role of Epidermal Growth Factor Receptor Signaling Pathway during Bovine Herpesvirus 1 Productive Infection in Cell Culture

Qiu

Chang

et al. 2020

Viruses

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Accumulating studies have shown that the epidermal growth factor receptor (EGFR) signaling pathway plays an essential role in mediating cellular entry of numerous viruses. In this study, we report that bovine herpesvirus 1 (BoHV-1) productive infection in both the human lung carcinoma cell line A549 and bovine kidney (MDBK) cells leads to activation of EGFR, as demonstrated by the increased phosphorylation of EGFR at Tyr1068 (Y1068), which in turn plays important roles in virus infection. A time-of-addition assay supported that virus replication at post-entry stages was affected by the EGFR specific inhibitor Gefitinib. Interestingly, both phospholipase C-γ1 (PLC-γ1) and Akt, canonical downstream effectors of EGFR, were activated following virus infection in A549 cells, while Gefitinib could inhibit the activation of PLC-γ1 but not Akt. In addition, virus titers in A549 cells was inhibited by chemical inhibition of PLC-γ1, but not by the inhibition of Akt. However, the Akt specific inhibitor Ly294002 could significantly reduce the virus titer in MDBK cells. Taken together, our data suggest that PLC-γ1 is stimulated in part through EGFR for efficient replication in A549 cells, whereas Akt can be stimulated by virus infection independent of EGFR, and is not essential for virus productive infection, indicating that Akt modulates BoHV-1 replication in a cell type-dependent manner. This study provides novel insights on how BoHV-1 infection activates EGFR signaling transduction to facilitate virus replication.

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Section: Introductionmentioning

confidence: 99%

The Role of Epidermal Growth Factor Receptor Signaling Pathway during Bovine Herpesvirus 1 Productive Infection in Cell Culture

Qiu

Chang

et al. 2020

Viruses

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“…In HSV-1 infected murine microglial cells, ROS mediated the regulation of some inflammation pertinent signaling, such as p38MAPK and Erk1/2 pathways [ 13 ]. In contrast, the activation of p38MAPK and Erk1/2 signaling by BoHV-1 infection is not mediated by over-produced ROS [ 14 ], though BoHV-1 and HSV-1 are genetically closed [ 9 ]. How BoHV-1 infection contributes to ROS production and the activation of p38MAPK and Erk1/2 signaling has yet to be found.…”

Section: Introductionmentioning

confidence: 99%

The role of phospholipase C signaling in bovine herpesvirus 1 infection

Zhu

Yuan

Ding

et al. 2017

Vet Res

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Bovine herpesvirus 1 (BoHV-1) infection enhanced the generation of inflammatory mediator reactive oxidative species (ROS) and stimulated MAPK signaling that are highly possibly related to virus induced inflammation. In this study, for the first time we show that BoHV-1 infection manipulated phospholipase C (PLC) signaling, as demonstrated by the activation of PLCγ-1 at both early stages [at 0.5 h post-infection (hpi)] and late stages (4–12 hpi) during the virus infection of MDBK cells. Viral entry, and de novo protein expression and/or DNA replication were potentially responsible for the activation of PLCγ-1 signaling. PLC signaling inhibitors of both U73122 and edelfosine significantly inhibited BoHV-1 replication in both bovine kidney cells (MDBK) and rabbit skin cells (RS-1) in a dose-dependent manner by affecting the virus entry stage(s). In addition, the activation of Erk1/2 and p38MAPK signaling, and the enhanced generation of ROS by BoHV-1 infection were obviously ameliorated by chemical inhibition of PLC signaling, implying the requirement of PLC signaling in ROS production and these MAPK pathway activation. These results suggest that the activation of PLC signaling is a potential pathogenic mechanism for BoHV-1 infection.

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“…It has been reported that c-Jun-dependent trans-activation supports HSV-1 replication in cell cultures ( McLean and Bachenheimer, 1999 ). Similarly, BoHV-1 infection activates the JNK/c-Jun cascade, with inhibition of this pathway via the chemical inhibitor SP600125 significantly blocking productive infection in cell cultures ( Zhu et al, 2016 ). However, how c-Jun signaling is affected by virus infection remains poorly understood.…”

Section: Introductionmentioning

confidence: 99%

β-cantenin is potentially involved in the regulation of c-Jun signaling following bovine herpesvirus 1 infection

Chang

Yuan

Zhu

2020

Veterinary Microbiology

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Highlights BoHV-1 infection promotes nucleus accumulation of p-c-Jun(S73) and p-β-catenin(S552) The association between β-catenin and c-Jun in in nucleus is readily detected following BoHV-1 infection. BoHV-1 infection stimulates the expression and activation of c-Jun potentially through β-catenin. BoHV-1 infection leads to relocalization of nucleus c-Jun to form specific foci.

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The activation of p38MAPK and JNK pathways in bovine herpesvirus 1 infected MDBK cells

Cited by 14 publications

References 38 publications

The Role of Epidermal Growth Factor Receptor Signaling Pathway during Bovine Herpesvirus 1 Productive Infection in Cell Culture

The Role of Epidermal Growth Factor Receptor Signaling Pathway during Bovine Herpesvirus 1 Productive Infection in Cell Culture

The role of phospholipase C signaling in bovine herpesvirus 1 infection

β-cantenin is potentially involved in the regulation of c-Jun signaling following bovine herpesvirus 1 infection

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