Evidence map›Paper›PMID 23981351›Full record

ArticleBioinformatics (Oxford, England)2013

A combined omics study on activated macrophages--enhanced role of STATs in apoptosis, immunity and lipid metabolism.

Ashok Reddy Dinasarapu, Shakti Gupta, Mano Ram Maurya, Eoin Fahy, Jun Min, Manish Sud, Merril J Gersten, Christopher K Glass, Shankar Subramaniam

Open access · bronzeAbstract read
In one paragraph

Article in Bioinformatics (Oxford, England), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

17 citing papers in PubMed, 34 citations in OpenAlex.

  1. Sp140L functions as a herpesvirus restriction factor suppressing viral transcription and activating interferon-stimulated genes.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  2. Review
  3. An adaptableMolecular omics · 2024
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  4. Review
  5. Macrophage Cell Cycle.Results and problems in cell differentiation · 2024
    Review
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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

9 authors at 3 institutions in 2 countries.

Ashok Reddy DinasarapuDepartment of Bioengineering, San Diego Super Computer Center, Department of Cellular and Molecular Medicine and Department of Chemistry and Biochemistry, University of California San Diego, CA 92093, USA.
Shakti Gupta
Mano Ram Maurya
Eoin Fahy
Jun Min
Manish Sud
Merril J Gersten
Christopher K Glass
Shankar Subramaniam
University of California San Diego · USSan Diego Supercomputer Center · USUniversity of San Diego · US

Funding

STEROL LIPIDSU54GM069338 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI DENNIS, EDWARD A · 2003 to 2013
$72.2M
Transcriptional Genomics CoreP01DK074868 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GLASS, CHRISTOPHER K · 2007 to 2016
$16.6M
LIPID Metabolites And Pathways Strategy (LIPID MAPS)R24GM107784 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI FAHY, EOIN · 2013 to 2015
$1.5M
NIDDK NIH HHS P01-DK074868NIGMS NIH HHS R24 GM107784NIGMS NIH HHS U54 GM069338NIGMS NIH HHS U54 GM69338-04
6 · The paper itself

Abstract

backgroundMacrophage activation by lipopolysaccharide and adenosine triphosphate (ATP) has been studied extensively because this model system mimics the physiological context of bacterial infection and subsequent inflammatory responses. Previous studies on macrophages elucidated the biological roles of caspase-1 in post-translational activation of interleukin-1β and interleukin-18 in inflammation and apoptosis. However, the results from these studies focused only on a small number of factors. To better understand the host response, we have performed a high-throughput study of Kdo2-lipid A (KLA)-primed macrophages stimulated with ATP.

resultsThe study suggests that treating mouse bone marrow-derived macrophages with KLA and ATP produces 'synergistic' effects that are not seen with treatment of KLA or ATP alone. The synergistic regulation of genes related to immunity, apoptosis and lipid metabolism is observed in a time-dependent manner. The synergistic effects are produced by nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) and activator protein (AP)-1 through regulation of their target cytokines. The synergistically regulated cytokines then activate signal transducer and activator of transcription (STAT) factors that result in enhanced immunity, apoptosis and lipid metabolism; STAT1 enhances immunity by promoting anti-microbial factors; and STAT3 contributes to downregulation of cell cycle and upregulation of apoptosis. STAT1 and STAT3 also regulate glycerolipid and eicosanoid metabolism, respectively. Further, western blot analysis for STAT1 and STAT3 showed that the changes in transcriptomic levels were consistent with their proteomic levels. In summary, this study shows the synergistic interaction between the toll-like receptor and purinergic receptor signaling during macrophage activation on bacterial infection. AVAILABILITY: Time-course data of transcriptomics and lipidomics can be queried or downloaded from http://www.lipidmaps.org. CONTACT: shankar@ucsd.edu. SUPPLEMENTARY INFORMATION: Supplementary data are available at Bioinformatics online.

Indexed as

Gene Expression ProfilingAnimalsApoptosisCell CycleCytokinesImmunityLipid MetabolismLipopolysaccharidesMacrophage ActivationMacrophagesMiceNF-kappa BProteomicsSignal TransductionSTAT1 Transcription FactorSTAT3 Transcription FactorCytokinesKdo2-lipid ALipopolysaccharidesNF-kappa BSTAT1 Transcription FactorSTAT3 Transcription FactorToll-Like Receptors

Identifiers

PMID23981351
PMCPMC3799469
OpenAlexW2139163144

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.