Evidence map›Paper›PMID 30241502›Full record

ArticleBMC neuroscience2018

Anti-inflammatory effects of minocycline are mediated by retinoid signaling.

Vera Clemens, Francesca Regen, Nathalie Le Bret, Isabella Heuser, Julian Hellmann-Regen

Open access · goldAbstract read
In one paragraph

Article in BMC neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 18% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

  1. Pooled it
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  3. 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

5 authors at 1 institution in 1 country.

Vera ClemensSection Clinical Neurobiology, Department of Psychiatry and Psychotherapy, Campus Benjamin Franklin, Charité - University Medicine Berlin, Hindenburgdamm 30, 12203, Berlin, Germany. vera.clemens@charite.de.
Francesca RegenSection Clinical Neurobiology, Department of Psychiatry and Psychotherapy, Campus Benjamin Franklin, Charité - University Medicine Berlin, Hindenburgdamm 30, 12203, Berlin, Germany.
Nathalie Le BretSection Clinical Neurobiology, Department of Psychiatry and Psychotherapy, Campus Benjamin Franklin, Charité - University Medicine Berlin, Hindenburgdamm 30, 12203, Berlin, Germany.
Isabella HeuserSection Clinical Neurobiology, Department of Psychiatry and Psychotherapy, Campus Benjamin Franklin, Charité - University Medicine Berlin, Hindenburgdamm 30, 12203, Berlin, Germany.
Julian Hellmann-RegenSection Clinical Neurobiology, Department of Psychiatry and Psychotherapy, Campus Benjamin Franklin, Charité - University Medicine Berlin, Hindenburgdamm 30, 12203, Berlin, Germany.
Charité - Universitätsmedizin Berlin · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMinocycline is a lipophilic tetracycline of increasing appeal in neuroscience as it inhibits microglial activation, a mechanism involved in numerous neuropsychiatric disorders. Own data point towards retinoid-mediated effects of minocycline in murine brain and skin, and towards a vicious cycle of neuroinflammation which is driven by microglial activation-induced breakdown of local retinoids such as retinoic acid (RA). We therefore sought to study minocycline's anti-inflammatory effects on human microglial-like monocyte-derived cells in the context of retinoid signaling.

resultsAs hypothesized, minocycline exposure resulted in a substantial increase of RA levels in the human monocytic cell line THP-1. While pro-inflammatory stimulation with lipopolysaccharides resulted in increased tryptophane-degrading indoleamine-2,3-dioxygenase IDO-expression and TNF-α levels in primary human monocyte-derived microglial-like cells, this effect was attenuated by minocycline only in the presence of retinoids. The anti-inflammatory effects of minocycline on TNF-α expression were completely abolished by a pharmacological blockage of retinoic acid receptors (RARs) using BMS-493 and unaffected by selectively blocking retinoid-X-receptors using UVI-3003.

conclusionsOur data indicate for the first time a RA-dependent, anti-inflammatory effect for minocycline in human microglial-like cells via inhibition of local RA turnover. The RA-dependent mode of action for minocycline appears to be predominantly mediated through RAR-signaling.

Indexed as

Anti-Inflammatory Agents, Non-SteroidalBenzoatesCoumaric AcidsHumansIndoleamine-Pyrrole 2,3,-DioxygenaseInterleukin-6Kynurenine 3-MonooxygenaseLipopolysaccharidesMacrophagesMicrogliaMinocyclineMonocytesReceptors, Retinoic AcidStilbenesTetrahydronaphthalenesTHP-1 Cells4-(2-(5,6-dihydro-5,5-dimethyl-8-(2-phenylethynyl)naphthalen-2-yl)ethen-1-yl)benzoic acidAnti-Inflammatory Agents, Non-SteroidalBenzoatesCoumaric AcidsIL6 protein, humanIndoleamine-Pyrrole 2,3,-DioxygenaseInterleukin-6Kynurenine 3-MonooxygenaseLipopolysaccharidesMinocyclineReceptors, Retinoic AcidStilbenesTetrahydronaphthalenesTNF protein, humanTretinoinTumor Necrosis Factor-alphaUVI 3003CytokinesMicrogliaMinocyclineNeuroinflammationRetinoic acid

Identifiers

PMID30241502
PMCPMC6151010
OpenAlexW2890267216

What OpenQuestion holds

Textmetadata
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.