Evidence map›Paper›PMID 34823472›Full record

ArticleBMC genomics2021

RNAseq analysis of treatment-dependent signaling changes during inflammation in a mouse cutaneous wound healing model.

Georges St Laurent, Ian Toma, Bernd Seilheimer, Konstantin Cesnulevicius, Myron Schultz, Michael Tackett, Jianhua Zhou, Maxim Ri, Dmitry Shtokalo, Denis Antonets and 2 more

Open access · goldAbstract read
In one paragraph

Article in BMC genomics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

7 citing papers in PubMed, 13 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

12 authors at 5 institutions in 3 countries.

Georges St LaurentThe St. Laurent Institute, Vancouver, WA, USA.
Ian TomaDepartment of Medicine, Division of Genomic Medicine, The George Washington University Medical Center, 2300 Eye St, Washington D.C, 20037, USA.
Bernd SeilheimerHeel GmbH, Baden-Baden, Germany.
Konstantin CesnuleviciusHeel GmbH, Baden-Baden, Germany.
Myron SchultzHeel GmbH, Baden-Baden, Germany.
Michael TackettThe St. Laurent Institute, Vancouver, WA, USA.
Jianhua ZhouThe St. Laurent Institute, Vancouver, WA, USA.
Maxim RiThe St. Laurent Institute, Vancouver, WA, USA.
Dmitry ShtokaloThe St. Laurent Institute, Vancouver, WA, USA.
Denis AntonetsAcademGene, LLC, Novosibirsk, Russia.
Tisha JepsonThe St. Laurent Institute, Vancouver, WA, USA.
Timothy A McCaffreyDepartment of Medicine, Division of Genomic Medicine, The George Washington University Medical Center, 2300 Eye St, Washington D.C, 20037, USA. mcc@gwu.edu.
St. Laurent Institute · USHeel (Germany) · DEGeorge Washington University · USInstitute of Informatics Problems · RUWashington University Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDespite proven therapeutic effects in inflammatory conditions, the specific mechanisms of phytochemical therapies are not well understood. The transcriptome effects of Traumeel (Tr14), a multicomponent natural product, and diclofenac, a non-selective cyclooxygenase (COX) inhibitor, were compared in a mouse cutaneous wound healing model to identify both known and novel pathways for the anti-inflammatory effect of plant-derived natural products.

methodsSkin samples from abraded mice were analyzed by single-molecule, amplification-free RNAseq transcript profiling at 7 points between 12 and 192 h after injury. Immediately after injury, the wounds were treated with either diclofenac, Tr14, or placebo control (n = 7 per group/time). RNAseq levels were compared between treatment and control at each time point using a systems biology approach.

resultsAt early time points (12-36 h), both control and Tr14-treated wounds showed marked increase in the inducible COX2 enzyme mRNA, while diclofenac-treated wounds did not. Tr14, in contrast, modulated lipoxygenase transcripts, especially ALOX12/15, and phospholipases involved in arachidonate metabolism. Notably, Tr14 modulated a group of cell-type specific markers, including the T cell receptor, that could be explained by an overarching effect on the type of cells that were recruited into the wound tissue.

conclusionsTr14 and diclofenac had very different effects on the COX/LOX synthetic pathway after cutaneous wounding. Tr14 allowed normal autoinduction of COX2 mRNA, but suppressed mRNA levels for key enzymes in the leukotriene synthetic pathway. Tr14 appeared to have a broad 'phytocellular' effect on the wound transcriptome by altering the balance of cell types present in the wound.

Indexed as

InflammationWound HealingAnimalsAnti-Inflammatory Agents, Non-SteroidalBiomarkersDiclofenacMiceAnti-Inflammatory Agents, Non-SteroidalBiomarkersDiclofenacCyclooxygenaseDiclofenacInflammationLipoxygenasePhospholipaseRNA sequencingTranscriptomeTraumeel

Identifiers

PMID34823472
PMCPMC8614049
OpenAlexW3159210473

What OpenQuestion holds

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LicenceCC BY
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.