Yin Yang 1 Dynamically Regulates Antiviral Innate Immune Responses During Viral Infection

Zan, Jie; Zhang, Hao; Gu, Aiping; Zhong, Kailun; Lu, Michael L.; Bai, Xiaoxin; Zhang, Jinyang; Cai, Jun

doi:10.1159/000485116

Cited by 25 publications

(17 citation statements)

References 39 publications

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“…Josse and colleagues suggested that this effect could be mediated by binding of YY1 to the proximal promoter. Furthermore, YY1 interacts also in the absence of viral infection in mice with the signal transducer and activator of transcription 1 (STAT1), one of the main factors mediating ISG expression [ 35 ], implying important roles of YY proteins at different stages during infection [ 120 ]. In the human cell, YY1 and YY2 regulate enhanceosome formation from YY-binding site-containing regions far upstream of the TSS of the IFNB1 gene at −3 kb and −2 kb, termed DNase I hypersensitive sites 1 (HS1) and HS2, respectively [ 121 ].…”

Section: A Complex Performance—stimulus-induced Assembly Of the Ifmentioning

confidence: 99%

Of Keeping and Tipping the Balance: Host Regulation and Viral Modulation of IRF3-Dependent IFNB1 Expression

Schwanke

Stempel

Brinkmann

2020

Viruses

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The type I interferon (IFN) response is a principal component of our immune system that allows to counter a viral attack immediately upon viral entry into host cells. Upon engagement of aberrantly localised nucleic acids, germline-encoded pattern recognition receptors convey their find via a signalling cascade to prompt kinase-mediated activation of a specific set of five transcription factors. Within the nucleus, the coordinated interaction of these dimeric transcription factors with coactivators and the basal RNA transcription machinery is required to access the gene encoding the type I IFN IFNβ (IFNB1). Virus-induced release of IFNβ then induces the antiviral state of the system and mediates further mechanisms for defence. Due to its key role during the induction of the initial IFN response, the activity of the transcription factor interferon regulatory factor 3 (IRF3) is tightly regulated by the host and fiercely targeted by viral proteins at all conceivable levels. In this review, we will revisit the steps enabling the trans-activating potential of IRF3 after its activation and the subsequent assembly of the multi-protein complex at the IFNβ enhancer that controls gene expression. Further, we will inspect the regulatory mechanisms of these steps imposed by the host cell and present the manifold strategies viruses have evolved to intervene with IFNβ transcription downstream of IRF3 activation in order to secure establishment of a productive infection.

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Section: A Complex Performance—stimulus-induced Assembly Of the Ifmentioning

confidence: 99%

Of Keeping and Tipping the Balance: Host Regulation and Viral Modulation of IRF3-Dependent IFNB1 Expression

Schwanke

Stempel

Brinkmann

2020

Viruses

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“…The miR-148a-3p and Rock2 luciferase reporter assays were identical to those described above. [35,36]. The RT-PCR primer sequence was synthesized by Generay (oligo sequences are shown in Table 1).…”

Section: Tunel (Terminal Deoxynucleotidyl Transferase Dutpmentioning

confidence: 99%

Metformin Protects against Oxidative Stress Injury Induced by Ischemia/Reperfusion via Regulation of the lncRNA-H19/miR-148a-3p/Rock2 Axis

Zeng

Zhu

Liu

et al. 2019

Oxidative Medicine and Cellular Longevity

Self Cite

110

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Previous studies have shown that metformin not only is a hypoglycemic agent but also has neuroprotective effects. However, the mechanism of action of metformin in ischemic stroke is unclear. Oxidative stress is an important factor in the pathogenesis of cerebral ischemia-reperfusion injury. It has been reported that metformin is associated with stroke risk in the clinical population. This study is aimed at investigating the effect and mechanism of metformin in an experimental model of oxidative stress induced by ischemia/reperfusion (I/R) in vivo and oxygen glucose deprivation/reperfusion (OGD/R) in vitro. Metformin (100, 200, and 300 mg/kg) was administered intraperitoneally immediately after induction of cerebral ischemia. The indicators of oxidative stress selected were antioxidant enzyme activities of catalase, malondialdehyde (MDA), nitric oxide (NO), superoxide dismutase (SOD), and glutathione peroxidation enzyme (GSHPx). First, we demonstrated that metformin can significantly alleviate acute and chronic cerebral I/R injury and it has a strong regulatory effect on stroke-induced oxidative stress. It can reduce the elevated activities of MDA and NO and increase the levels of GSHPx and SOD in the cerebrum of mice and N2a cells exposed to I/R. Furthermore, real-time PCR and western blot were used to detect the expression of long noncoding RNA H19 (lncRNA-H19), microRNA-148a-3p (miR-148a-3p), and Rho-associated protein kinase 2 (Rock2). The direct interaction of lncRNA-H19, miR-148a-3p, and Rock2 was tested using a dual luciferase reporter assay. lncRNA-H19 altered OGD/R-induced oxidative stress by modulating miR-148a-3p to increase Rock2 expression. The expression of lncRNA-H19 and Rock2 could be downregulated with metformin in vivo and in vitro. In conclusion, our study confirmed that metformin exerts neuroprotective effects by regulating ischemic stroke-induced oxidative stress injury via the lncRNA-H19/miR-148a-3p/Rock2 axis. These results provide new evidence that metformin may represent a potential treatment for stroke-related brain injury.

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“…Activation gives rise to the activation of ISGs via recognition of upstream sequence elements in promoters and formation of antiviral proteins such as OAS, PKR, ISG and Mx, which exert distinct biological activities (Fig. 1) [2, 12-14]. The differences among type I IFN classes is prominent compared to these common points.…”

Section: Biological Activities Of Type I Ifnsmentioning

confidence: 99%

Type I Interferons: Distinct Biological Activities and Current Applications for Viral Infection

Gong

Zhao

et al. 2018

Cell Physiol Biochem

141

111

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The interferons (IFNs) are a primary defense against pathogens because of the strong antiviral activities they induce. IFNs can be classified into three groups: type I, type II and type III, according to their genetic, structural, and functional characteristics and their receptors on the cell surface. The type I IFNs are the largest group and include IFN-α, IFN-β, IFN-ε, IFN-ω, IFN-κ, IFN-δ, IFN-τ and IFN-ζ. The use of IFNs for the treatment of viral infectious diseases on their antiviral activity may become an important therapeutic option, for example, IFN-α is well known for the successful treatment of hepatitis B and C virus infections, and interest is increasing in the antiviral efficacy of other novel IFN classes and their potential applications. Therefore, in this review, we summarize the recent progress in the study of the biological activities of all the type I IFN classes and their potential applications in the treatment of infections with immunodeficiency virus, hepatitis viruses, and influenza viruses.

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Yin Yang 1 Dynamically Regulates Antiviral Innate Immune Responses During Viral Infection

Cited by 25 publications

References 39 publications

Of Keeping and Tipping the Balance: Host Regulation and Viral Modulation of IRF3-Dependent IFNB1 Expression

Of Keeping and Tipping the Balance: Host Regulation and Viral Modulation of IRF3-Dependent IFNB1 Expression

Metformin Protects against Oxidative Stress Injury Induced by Ischemia/Reperfusion via Regulation of the lncRNA-H19/miR-148a-3p/Rock2 Axis

Type I Interferons: Distinct Biological Activities and Current Applications for Viral Infection

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