Evidence map›Paper›PMID 25248747›Full record

ArticleThe Journal of biological chemistry2014

Reduced levels of microRNAs miR-124a and miR-150 are associated with increased proinflammatory mediator expression in Krüppel-like factor 2 (KLF2)-deficient macrophages.

Palanikumar Manoharan, Joshua E Basford, Robyn Pilcher-Roberts, Jonathan Neumann, David Y Hui, Jerry B Lingrel

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

28 citing papers in PubMed, 59 citations in OpenAlex.

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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

6 authors at 1 institution in 1 country.

Palanikumar ManoharanFrom the Departments of Molecular Genetics, Biochemistry, and Microbiology and.
Joshua E BasfordPathology and Laboratory Medicine, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267.
Robyn Pilcher-RobertsFrom the Departments of Molecular Genetics, Biochemistry, and Microbiology and.
Jonathan NeumannFrom the Departments of Molecular Genetics, Biochemistry, and Microbiology and.
David Y HuiPathology and Laboratory Medicine, University of Cincinnati College of Medicine, Cincinnati, Ohio 45267.
Jerry B LingrelFrom the Departments of Molecular Genetics, Biochemistry, and Microbiology and lingrejb@ucmail.uc.edu.
University of Cincinnati Medical Center · US

Funding

LCenter for Clinical and Translational Science and TrainingUL1TR001425 · NCATS · UNIVERSITY OF CINCINNATI · PI HEUBI, JAMES E., KISSELA, BRETT M · 2015 to 2024
$37.5M
Cincinnati Center for Clinical and Translational Sciences and TrainingUL1TR000077 · NCATS · UNIVERSITY OF CINCINNATI · PI HEUBI, JAMES E. · 2012 to 2014
$9.9M
Role of Lipoprotein Receptors in Diet-induced Obesity and DiabetesR01DK074932 · NIDDK · UNIVERSITY OF CINCINNATI · PI HUI, DAVID YIU-KWAN · 2007 to 2019
$4.4M
The Role of the KLF2 in Vascular Endothelial CellsR01HL078806 · NHLBI · UNIVERSITY OF CINCINNATI · PI LINGREL, JERRY B · 2007 to 2010
$1.6M
NCATS NIH HHS UL1 TR000077NCATS NIH HHS UL1 TR001425NHLBI NIH HHS HL78806NHLBI NIH HHS R01 HL078806NIDDK NIH HHS DK74932NIDDK NIH HHS R01 DK074932
6 · The paper itself

Abstract

Previous studies have shown that the myeloid-specific deficiency of the transcription factor Krüppel-like factor 2 (KLF2) accelerates atherosclerosis in hypercholesterolemic Ldlr(-/-) mice due to the enhanced adhesion of myeloid cells to activated endothelial cells in the vessel wall. This study revealed elevated basal inflammation with elevated plasma levels of Ccl2, Ccl4, Ccl5, and Ccl11 in the myeloid-specific KLF2 knock-out (myeKlf2(-/-)) mice. Peritoneal macrophages isolated from myeKlf2(-/-) mice showed increased mRNA levels of several inflammatory mediators, including Ccl2, Ccl5, Ccl7, Cox-2, Cxcl1, and IL-6. In contrast, the levels of two microRNAs, miR-124a and miR-150, were lower in Klf2(-/-) macrophages compared with Klf2(+/+) macrophages. Additional studies showed a direct inverse relationship between miR-124a levels with Ccl2 expression, with anti-miR-124a increasing Ccl2 mRNA levels in Klf2(+/+) macrophages, whereas the restoration of miR-124a levels in Klf2(-/-) macrophages significantly reduced Ccl2 mRNA expression. Likewise, the inverse relationship was observed between miR-150 levels and Cxcl1 expression in Klf2(+/+) and Klf2(-/-) mice. Moreover, miR150 likely regulates the miR124a expression and thus augments expression of inflammatory mediators in myeKlf2(-/-) macrophages. This study documented that the transcription factor KLF2 modulates inflammatory chemokine production via regulation of microRNA expression levels in immune cells.

Indexed as

Gene Expression RegulationAnimalsAtherosclerosisBase SequenceBinding SitesChemokinesFemaleInflammationKruppel-Like Transcription FactorsMacrophages, PeritonealMiceMice, Inbred C57BLMice, KnockoutMicroRNAsMolecular Sequence DataMyeloid CellsChemokinesKlf2 protein, mouseKruppel-Like Transcription FactorsMicroRNAsMirn124 microRNA, mouseMirn150 microRNA, mouseChemokineInflammationKruppel-like Factor 2 (KLF2)MacrophageMicroRNA (miRNA)

Identifiers

PMID25248747
PMCPMC4223359
OpenAlexW1999333735

What OpenQuestion holds

Textmetadata
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.