Evidence map›Paper›PMID 37212859›Full record

ArticleJournal of molecular medicine (Berlin, Germany)2023

Dysregulation of miRNA-30e-3p targeting IL-1β in an international cohort of systemic autoinflammatory disease patients.

Tayfun Hilmi Akbaba, Yeliz Z Akkaya-Ulum, Ezgi Deniz Batu, Federica Penco, Helmut Wittkowski, Benjamin Kant, Marielle E van Gijn, Dirk Foell, Marco Gattorno, Seza Ozen and 1 more

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In one paragraph

Article in Journal of molecular medicine (Berlin, Germany), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

5 citing papers in PubMed, 9 citations in OpenAlex.

  1. 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

11 authors at 5 institutions in 4 countries.

Tayfun Hilmi AkbabaDepartment of Medical Biology, Faculty of Medicine, Hacettepe University, Ankara, Turkey.ORCID 0000-0002-3875-5244
Yeliz Z Akkaya-UlumDepartment of Medical Biology, Faculty of Medicine, Hacettepe University, Ankara, Turkey.
Ezgi Deniz BatuDepartment of Pediatric Rheumatology, Faculty of Medicine, Hacettepe University, Ankara, Turkey.
Federica PencoUnit of Rheumatology and Autoinflammatory Diseases, IRCCS Istituto Giannina Gaslini, Genova, Italy.
Helmut WittkowskiDepartment for Pediatric Rheumatology & Immunology, University Hospital Muenster, Muenster, Germany.
Benjamin KantDepartment of Medical Genetics, University Medical Center Utrecht, Utrecht, Netherlands.
Marielle E van GijnDepartment of Medical Genetics, University Medical Center Utrecht, Utrecht, Netherlands.
Dirk FoellDepartment for Pediatric Rheumatology & Immunology, University Hospital Muenster, Muenster, Germany.
Marco GattornoDepartment of Medical Genetics, University Medical Center Utrecht, Utrecht, Netherlands.
Seza OzenDepartment of Pediatric Rheumatology, Faculty of Medicine, Hacettepe University, Ankara, Turkey.
Banu Balci-PeynirciogluDepartment of Medical Biology, Faculty of Medicine, Hacettepe University, Ankara, Turkey. banupeynir@yahoo.com.ORCID 0000-0002-8627-8796
Hacettepe University · TRUniversity Hospital Münster · DEUniversity Medical Center Utrecht · NLIstituto Giannina Gaslini · ITUniversity Medical Center Groningen · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autoinflammation is the standard mechanism seen in systemic autoinflammatory disease (SAID) patients. This study aimed to investigate the effect of a candidate miRNA, miR-30e-3p, which was identified in our previous study, on the autoinflammation phenotype seen in SAID patients and to analyze its expression in a larger group of European SAID patients. We examined the potential anti-inflammatory effect of miR-30e-3p, which we had defined as one of the differentially expressed miRNAs in microarray analysis involved in inflammation-related pathways. This study validated our previous microarray results of miR-30e-3p in a cohort involving European SAID patients. We performed cell culture transfection assays for miR-30e-3p. Then, in transfected cells, we analyzed expression levels of pro-inflammatory genes; IL-1β, TNF-α, TGF-β, and MEFV. We also performed functional experiments, caspase-1 activation by fluorometric assay kit, apoptosis assay by flow cytometry, and cell migration assays by wound healing and filter system to understand the possible effect of miR-30e-3p on inflammation. Following these functional assays, 3'UTR luciferase activity assay and western blotting were carried out to identify the target gene of the aforementioned miRNA. MiR-30e-3p was decreased in severe European SAID patients like the Turkish patients. The functional assays associated with inflammation suggested that miR-30e-3p has an anti-inflammatory effect. 3'UTR luciferase activity assay demonstrated that miR-30e-3p directly binds to interleukin-1-beta (IL-1β), one of the critical molecules of inflammatory pathways, and reduces both RNA and protein levels of IL-1β. miR-30e-3p, which has been associated with IL-1β, a principal component of inflammation, might be of potential diagnostic and therapeutic value for SAIDs. KEY MESSAGES: miR-30e-3p, which targets IL-1β, could have a role in the pathogenesis of SAID patients. miR-30e-3p has a role in regulating inflammatory pathways like migration, caspase-1 activation. miR-30e-3p has the potential to be used for future diagnostic and therapeutic approaches.

Indexed as

Hereditary Autoinflammatory DiseasesMicroRNAs3' Untranslated RegionsAnti-Inflammatory AgentsCaspasesHumansInflammationInterleukin-1betaLuciferasesPyrin3' Untranslated RegionsAnti-Inflammatory AgentsCaspasesInterleukin-1betaLuciferasesMEFV protein, humanMicroRNAsPyrinFamilial Mediterranean feverIL-1βInflammationMicroRNAmiR-30e-3pSystemic autoinflammatory disease

Identifiers

PMID37212859
OpenAlexW4377221257

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.