Retinoic Acid-Inducible Gene-I Is Induced in Endothelial Cells by LPS and Regulates Expression of COX-2

Imaizumi, Tadaatsu; Aratani, Satoko; Nakajima, Takeshi; Carlson, Margaret; Matsumiya, Tomoh; Tanji, Kunikazu; Ookawa, Keizou; Yoshida, Hidemi; Tsuchida, Shigeki; McIntyre, Thomas M.; Prescott, Stephen M.; Zimmerman, Guy A.; Satoh, Kei

doi:10.1006/bbrc.2002.6650

Cited by 110 publications

(119 citation statements)

References 40 publications

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“…The disruption of Rig-I was confirmed by northern blotting with a Rig-I probe ( Figure 1D) and western blotting using a polyclonal antibody to Rig-I ( Figure 1E), respectively. It was found that Rig-I can be induced by IFNβ and LPS in various tissues and cell types [15,35], as shown in wild-type MEFs treated with IFNβ and splenocytes treated with LPS ( Figure 1D and 1E). By contrast, no signals were detected by northern and western blotting in Rig-I -/-MEFs and splenocytes even …”

Section: Targeted Disruption Of Rig-imentioning

confidence: 56%

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Rig-I−/− mice develop colitis associated with downregulation of Gαi2

et al. 2007

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Section: Targeted Disruption Of Rig-imentioning

confidence: 56%

“…Thus, RIG-I is thought to be the third pattern-recognition receptor in addition to TLRs and NLRs. Moreover, RIG-I can also regulate the transcription of many genes including interferon-γ stimulated gene 15 in MCF-7 cells and COX-2 in endothelial cells [14,15].…”

Section: Introductionmentioning

confidence: 99%

Rig-I−/− mice develop colitis associated with downregulation of Gαi2

et al. 2007

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“…NS5A protein was also detected using a polyclonal antibody to NS5A (Chiron, Emeryville, CA). RIG proteins were detected using a polyclonal antibody (25).…”

Section: Cells and Virusesmentioning

confidence: 99%

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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“…Both the magnitude and nature of these responses depended on the type of stimuli and the cell line tested. IFN-␥ (21), IL-1␤ (22), LPS (23) and dsRNA (24) increased RIG-I expression levels in vascular smooth muscle (21), endothelial cells (24), and fibroblasts (22). It was recently reported that IFN-␣ and TNF-␣ treatment enhanced virus-induced expression of IFN-␤ by activating RIG-I expression in the lung epithelial cell line A549 (2).…”

Section: Tnf-␣ Induces Rig-i Expression In Hela Cellsmentioning

confidence: 99%

IFN-ε Mediates TNF-α-Induced STAT1 Phosphorylation and Induction of Retinoic Acid-Inducible Gene-I in Human Cervical Cancer Cells

Matsumiya

Prescott

Stafforini

2007

The Journal of Immunology

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Retinoic acid inducible gene-I (RIG-I) plays important roles during innate immune responses to viral infections and as a transducer of cytokine signaling. The mechanisms of RIG-I up-regulation after cytokine stimulation are incompletely characterized. It was previously reported that IFN–γ induces the expression of RIG-I in endothelial cells. In this study, we characterized the mechanism of type I IFN-mediated up-regulation of RIG-I in HeLa cells and found that, in addition to type I IFN, TNF-α, a cytokine that regulates innate immune responses, induced expression of RIG-I. To investigate whether TNF-α- and type I IFN-mediated up-regulations of RIG-I were causally related, we studied the kinetics of these responses. Our results were consistent with a model in which TNF-α functioned upstream of type I IFNs. The ability of TNF-α to up-regulate RIG-I required protein synthesis, expression of functional type I IFNRs, and STAT1 signaling. We also found that IFN-ε was the only IFN isoform expressed constitutively in HeLa cells and that its expression was up-regulated in response to stimulation with TNF-α. The mechanism of up-regulation involved stabilization of IFN-ε mRNA in the absence of transcriptional activation. Silencing the expression of IFN-ε attenuated STAT1 expression and phosphorylation and inhibited RIG-I expression, providing additional support for the participation of IFN-ε upstream of STAT1. Our findings support a sequential mechanism whereby TNF-α leads to stabilization of IFN-ε mRNA, increased IFN-ε synthesis, engagement of type I IFNRs, increased STAT1 expression and phosphorylation, and up-regulation of RIG-I expression. These findings have implications for our understanding of the immune responses that follow cytokine stimulation.

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Retinoic Acid-Inducible Gene-I Is Induced in Endothelial Cells by LPS and Regulates Expression of COX-2

Cited by 110 publications

References 40 publications

Rig-I−/− mice develop colitis associated with downregulation of Gαi2

Rig-I−/− mice develop colitis associated with downregulation of Gαi2

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

IFN-ε Mediates TNF-α-Induced STAT1 Phosphorylation and Induction of Retinoic Acid-Inducible Gene-I in Human Cervical Cancer Cells

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