ArticleInflammatory bowel diseases2013
RNase-L deficiency exacerbates experimental colitis and colitis-associated cancer.
Article in Inflammatory bowel diseases, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 38 citations in OpenAlex.
- Endonucleolytic RNA cleavage drives changes in gene expression during the innate immune response.Cell reports · 2024Article
- Unraveling the Role of RNase L Knockout in Alleviating Immune Response Activation in Mice Bone Marrow after Irradiation.International journal of molecular sciences · 2024Article
- Occludin Regulates HIV-1 Infection by Modulation of the Interferon Stimulated OAS Gene Family.Molecular neurobiology · 2023Article
- Occludin regulates HIV-1 infection by modulation of the interferon stimulated OAS gene family.Research square · 2023Article
- Identification of Small Molecule Inhibitors of RNase L by Fragment-Based Drug Discovery.Journal of medicinal chemistry · 2022Article
- Article
- Activation of the antiviral factor RNase L triggers translation of non-coding mRNA sequences.Nucleic acids research · 2021Article
- Acute colitis during chronic experimental traumatic brain injury in mice induces dysautonomia and persistent extraintestinal, systemic, and CNS inflammation with exacerbated neurological deficits.Journal of neuroinflammation · 2021Article
- New advances in our understanding of the "unique" RNase L in host pathogen interaction and immune signaling.Cytokine · 2020Review
- IFN-γ restores the impaired function of RNase L and induces mitochondria-mediated apoptosis in lung cancer.Cell death & disease · 2019Article
- The Roles of Type I Interferon in Bacterial Infection.Cell host & microbe · 2016Review
- The Roles of RNase-L in Antimicrobial Immunity and the Cytoskeleton-Associated Innate Response.International journal of molecular sciences · 2016Review
- RNase L attenuates mitogen-stimulated gene expression via transcriptional and post-transcriptional mechanisms to limit the proliferative response.The Journal of biological chemistry · 2014Article
- Enteropathogenic Escherichia coli inhibits type I interferon- and RNase L-mediated host defense to disrupt intestinal epithelial cell barrier function.Infection and immunity · 2014Article
- Panax notoginseng attenuates experimental colitis in the azoxymethane/dextran sulfate sodium mouse model.Phytotherapy research : PTR · 2014Article
- Modulators affecting the immune dialogue between human immune and colon cancer cells.World journal of gastrointestinal oncology · 2014Review
- RNase-L control of cellular mRNAs: roles in biologic functions and mechanisms of substrate targeting.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2014Review
- Ribonuclease L and metal-ion-independent endoribonuclease cleavage sites in host and viral RNAs.Nucleic acids research · 2014Article
- Tumor suppressor activity of RIG-I.Molecular & cellular oncologyReview
- 2-5A-Mediated decay (2-5AMD): from antiviral defense to control of host RNA.Critical reviews in biochemistry and molecular biologyReview
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundThe endoribonuclease RNase-L is a type-I interferon (IFN)-regulated component of the innate immune response that functions in antiviral, antibacterial, and antiproliferative activities. RNase-L produces RNA agonists of RIG-I-like receptors, sensors of cytosolic pathogen-associated RNAs that induce cytokines including IFN-β. IFN-β and RIG-I-like receptors signaling mediate protective responses against experimental colitis and colitis-associated cancer and contribute to gastrointestinal homeostasis. Therefore, we investigated a role for RNase-L in murine colitis and colitis-associated cancer and its association with RIG-I-like receptors signaling in response to bacterial RNA.
methodsColitis was induced in wild type-deficient and RNase-L-deficient mice (RNase-L⁻/⁻) by administration of dextran sulfate sodium (DSS). Colitis-associated cancer was induced by DSS and azoxymethane (AOM). Histological analysis and immunohistochemistry were performed on colon tissue to analyze immune cell infiltration and tissue damage after induction of colitis. Expression of cytokines was measured by quantitative real-time-PCR and ELISA.
resultsDSS-treated RNase-L⁻/⁻ mice exhibited a significantly higher clinical score, delayed leukocyte infiltration, reduced expression of IFN-β, tumor necrosis factor α, interleukin-1β, and interleukin-18 at early times post-DSS exposure, and increased mortality as compared with wild-type mice. DSS/AOM-treated RNase-L⁻/⁻ mice displayed an increased tumor burden. Bacterial RNA triggered IFN-β production in an RNase-L-dependent manner and provided a potential mechanism by which RNase-L contributes to the gastrointestinal immune response to microbiota and protects against experimental colitis and colitis-associated cancer.
conclusionsRNase-L promotes the innate immune response to intestinal damage and ameliorates murine colitis and colitis-associated cancer. The RNase-L-dependent production of IFN-β stimulated by bacterial RNA may be a mechanism to protect against gastrointestinal inflammatory disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.