Stability of CXCL‐8 and Related AU‐Rich mRNAs in the Context of Hepatitis C Virus Replication In Vitro

Green, Jamison; Khabar, Khalid S.A.; Koo, Bon Chang A.; Williams, Bryan R.G.; Polyak, Stephen J.

doi:10.1086/500510

Cited by 19 publications

(25 citation statements)

References 46 publications

(67 reference statements)

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“…CXCL-8 mRNA was quantitated by real-time reverse transcriptase (RT)-PCR, as recently described (19). Dilutions of precisely quantitated CXCL-8 cDNA in the PCMGSNEO plasmid (64) (kindly provided by Naofumi Mukaida), ranging from 0 to 10 7 copies per tube, were run in triplicate to generate a standard curve, which served as a reference to calculate the CXCL-8 copy number based on the cycle threshold.…”

Section: Cells and Virusesmentioning

confidence: 99%

“…Furthermore, RIG-N expression was associated with a 2.1-fold increase in the half-life of CXCL-8 mRNA following TNF-␣ stimulation. Statistical comparison of the decay rates by a one-phase exponential model (19) showed that this difference is significant (P ϭ 0.03).…”

mentioning

confidence: 97%

“…CXCL-8 has been shown to be an important mediator of the inflammatory responses to many viruses and bacteria. For example, CXCL-8 is induced in response to the expression of the HCV NS5A protein (3, 4, 16, 50) and HCV replication (19). Moreover, CXCL-8 inhibits the antiviral actions of IFN-␣ (29), and recent studies indicate that CXCL-8 protein levels are associated with HCV replication (30).…”

mentioning

confidence: 99%

“…In addition to transcriptional activation, modulation of the half-life of CXCL-8 mRNA plays a major role in CXCL-8 induction in response to various stimuli. For example, TNF-␣ and virus induction of CXCL-8 involve mRNA stabilization (19,23,31,61) via the binding of regulatory proteins to AREs in the 3ЈUTR of the mRNA (1, 6, 9, 53). We therefore determined whether RIG-I induction of CXCL-8 also involves stabilization of CXCL-8 mRNA.…”

mentioning

confidence: 99%

“…Huh7 cells were transfected with plasmids expressing RIG-N or GFP and treated with TNF-␣ to induce CXCL-8 mRNA. Actinomycin D was added to cultures to stop transcription, and CXCL-8 mRNA was quantified by real-time RT-PCR (19). As shown in Fig.…”

mentioning

confidence: 99%

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Regulation of CXCL-8 (Interleukin-8) Induction by Double-Stranded RNA Signaling Pathways during Hepatitis C Virus Infection

Wagoner

Austin

Green

et al. 2007

J Virol

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Hepatitis C virus (HCV) infection induces the ␣-chemokine interleukin-8 (CXCL-8Hepatitis C virus (HCV) infects an estimated 3% or 170 million of the world's population and causes an estimated 476,000 deaths per year due to complications of end-stage liver disease (56,62). In the United States, about 1.8% of the general population or 4 million persons are infected. Of those acutely infected with HCV, approximately 85% develop chronic infection, and about 70% of these patients develop histological evidence of chronic liver disease. Moreover, viremia is not cleared in about 50% of infected patients treated with pegylated interferon (IFN)-ribavirin therapy, the current standard of care. Compounding this issue are the predictions that in the next 20 years, HCV-related complications, including hepatic decompensation, hepatocellular carcinoma, and liverrelated deaths, will increase by 106%, 81%, and 180%, respectively (12). Thus, chronic hepatitis C is a serious global medical problem necessitating effective treatment. Given the propensity of HCV for chronic infection, association with severe liver disease, and difficulty of treatment, many studies are focused on HCV-host interactions that contribute to HCV persistence and pathogenesis.

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Section: Cells and Virusesmentioning

confidence: 99%

mentioning

confidence: 97%

mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Regulation of CXCL-8 (Interleukin-8) Induction by Double-Stranded RNA Signaling Pathways during Hepatitis C Virus Infection

Wagoner

Austin

Green

et al. 2007

J Virol

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Post-transcriptional control during chronic inflammation and cancer: a focus on AU-rich elements

Khabar

2010

Cell. Mol. Life Sci.

146

140

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A considerable number of genes that code for AU-rich mRNAs including cytokines, growth factors, transcriptional factors, and certain receptors are involved in both chronic inflammation and cancer. Overexpression of these genes is affected by aberrations or by prolonged activation of several signaling pathways. AU-rich elements (ARE) are important cis-acting short sequences in the 3′UTR that mediate recognition of an array of RNA-binding proteins and affect mRNA stability and translation. This review addresses the cellular and molecular mechanisms that are common between inflammation and cancer and that also govern ARE-mediated post-transcriptional control. The first part examines the role of the ARE-genes in inflammation and cancer and sequence characteristics of AU-rich elements. The second part addresses the common signaling pathways in inflammation and cancer that regulate the ARE-mediated pathways and how their deregulations affect ARE-gene regulation and disease outcome.

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HCV modifies EGF signalling and upregulates production of CXCR2 ligands: Role in inflammation and antiviral immune response

Groepper

Rufinatscha

Schröder

et al. 2018

Journal of Hepatology

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Stability of CXCL‐8 and Related AU‐Rich mRNAs in the Context of Hepatitis C Virus Replication In Vitro

Abstract: The data suggest that increased CXCL-8 gene expression in the context of HCV replication involves posttranscriptional events.

Cited by 19 publications

References 46 publications

Regulation of CXCL-8 (Interleukin-8) Induction by Double-Stranded RNA Signaling Pathways during Hepatitis C Virus Infection

Regulation of CXCL-8 (Interleukin-8) Induction by Double-Stranded RNA Signaling Pathways during Hepatitis C Virus Infection

Post-transcriptional control during chronic inflammation and cancer: a focus on AU-rich elements

HCV modifies EGF signalling and upregulates production of CXCR2 ligands: Role in inflammation and antiviral immune response

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