Evidence map›Paper›PMID 26503952›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2015

MicroRNA-26b Modulates the NF-κB Pathway in Alveolar Macrophages by Regulating PTEN.

Li Zhang, Chaoqun Huang, Yujie Guo, Xuxu Gou, Myron Hinsdale, Pamela Lloyd, Lin Liu

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.2field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

35 citing papers in PubMed, 54 citations in OpenAlex.

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  10. The Roles of Host Noncoding RNAs inFrontiers in immunology · 2021
    Review
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  14. Review
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  17. Coelonin, an Anti-Inflammation Active Component ofInternational journal of molecular sciences · 2019
    Article
  18. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Li ZhangOklahoma Center for Respiratory and Infectious Diseases, Oklahoma State University, Stillwater, OK 74078; Lundberg-Kienlen Lung Biology and Toxicology Laboratory, Oklahoma State University, Stillwater, OK 74078; Department of Physiological Sciences, Oklahoma State University, Stillwater, OK 74078; and.ORCID http://orcid.org/0000-0002-2430-2041
Chaoqun HuangOklahoma Center for Respiratory and Infectious Diseases, Oklahoma State University, Stillwater, OK 74078; Lundberg-Kienlen Lung Biology and Toxicology Laboratory, Oklahoma State University, Stillwater, OK 74078; Department of Physiological Sciences, Oklahoma State University, Stillwater, OK 74078; and.
Yujie GuoOklahoma Center for Respiratory and Infectious Diseases, Oklahoma State University, Stillwater, OK 74078; Lundberg-Kienlen Lung Biology and Toxicology Laboratory, Oklahoma State University, Stillwater, OK 74078; Department of Physiological Sciences, Oklahoma State University, Stillwater, OK 74078; and.
Xuxu GouOklahoma Center for Respiratory and Infectious Diseases, Oklahoma State University, Stillwater, OK 74078; Lundberg-Kienlen Lung Biology and Toxicology Laboratory, Oklahoma State University, Stillwater, OK 74078; Department of Physiological Sciences, Oklahoma State University, Stillwater, OK 74078; and.ORCID http://orcid.org/0000-0002-4477-7183
Myron HinsdaleOklahoma Center for Respiratory and Infectious Diseases, Oklahoma State University, Stillwater, OK 74078; Department of Physiological Sciences, Oklahoma State University, Stillwater, OK 74078; and Department of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 74126.
Pamela LloydOklahoma Center for Respiratory and Infectious Diseases, Oklahoma State University, Stillwater, OK 74078; Department of Physiological Sciences, Oklahoma State University, Stillwater, OK 74078; and.
Lin LiuOklahoma Center for Respiratory and Infectious Diseases, Oklahoma State University, Stillwater, OK 74078; Lundberg-Kienlen Lung Biology and Toxicology Laboratory, Oklahoma State University, Stillwater, OK 74078; Department of Physiological Sciences, Oklahoma State University, Stillwater, OK 74078; and lin.liu@okstate.edu.ORCID http://orcid.org/0000-0002-4811-4897
Oklahoma State University · US

Funding

ZFC3H1 Regulation of Host Defense and Influenza A Virus PathogenesisP20GM103648 · NIGMS · OKLAHOMA STATE UNIVERSITY STILLWATER · PI PATRAUCHAN, MARIANNA M. A. · 2013 to 2022
$22.3M
miR-101 Control of Pulmonary FibrosisR01HL116876 · NHLBI · OKLAHOMA STATE UNIVERSITY STILLWATER · PI LIU, LIN · 2013 to 2016
$1.4M
NHLBI NIH HHS R01 HL116876NHLBI NIH HHS R01HL116876NIGMS NIH HHS P20 GM103648NIGMS NIH HHS P20GM103648PHS HHS 09PRE2300211
6 · The paper itself

Abstract

NF-κB is one of the best-characterized transcription factors, providing the link between early membrane-proximal signaling events and changes in many inflammatory genes. MicroRNAs are small noncoding RNAs that regulate gene expression at the posttranscriptional level. In this study, we evaluated the role of miR-26b in the LPS-induced inflammatory response in bovine alveolar macrophages (bAMs). LPS stimulation of bAMs upregulated miR-26b at 1 h and downregulated it at 6 and 36 h. Overexpression of miR-26b in bAMs enhanced the LPS-induced mRNA expression of proinflammatory cytokines and chemokines, including TNF-α, IL-1β, IL-8, and IL-10, but it directly inhibited that of IL-6. A similar trend was observed for the release of these cytokines and chemokines from bAMs. miR-26b directly bound the 3'-untranslated region of PTEN, leading to the reduction of PTEN protein in bAMs. miR-26b also enhanced the LPS-induced NF-κB signaling pathway, as revealed by increased NF-κB transcriptional activity and phosphorylation of p65, IκBα, IκB kinase, and Akt. Moreover, PTEN silencing increased the LPS-induced mRNA expression of TNF-α, IL-1β, IL-6, IL-8, and IL-10 and upregulated the NF-κB pathway. Taken together, we conclude that miR-26b participates in the inflammatory response of LPS-stimulated bAMs by modulating the NF-κB pathway through targeting PTEN.

Indexed as

3' Untranslated RegionsAnimalsBinding SitesCattleCells, CulturedDNA-Binding ProteinsGene Expression RegulationI-kappa B KinaseI-kappa B ProteinsInflammationInterleukin-10Interleukin-1betaInterleukin-6Interleukin-8LipopolysaccharidesMacrophages, Alveolar3' Untranslated RegionsDNA-Binding ProteinsI-kappa B KinaseI-kappa B ProteinsInterleukin-10Interleukin-1betaInterleukin-6Interleukin-8LipopolysaccharidesMicroRNAsNF-KappaB Inhibitor alphaProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseRNA, MessengerTranscription Factor RelATumor Necrosis Factor-alpha

Identifiers

PMID26503952
PMCPMC4655123
OpenAlexW2133132258

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.