Evidence map›Paper›PMID 37860007›Full record

ArticleFrontiers in immunology2023

LncRNA MALAT1/microRNA-30b axis regulates macrophage polarization and function.

Imran Ahmad, Raza Ali Naqvi, Araceli Valverde, Afsar R Naqvi

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
6.7field-weighted citation impact, top 3% 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

24 citing papers in PubMed, 28 citations in OpenAlex.

  1. Dicer-independent miR-451a is upregulated in periodontitis and potentiates inflammation by impairing macrophage polarization and SOCS activity.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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  6. Noncoding RNAs in periodontitis: Progress and perspectives (Review).International journal of molecular medicine · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Imran AhmadMucosal Immunology Lab, College of Dentistry, University of Illinois at Chicago, Chicago, IL, United States.
Raza Ali NaqviMucosal Immunology Lab, College of Dentistry, University of Illinois at Chicago, Chicago, IL, United States.
Araceli ValverdeMucosal Immunology Lab, College of Dentistry, University of Illinois at Chicago, Chicago, IL, United States.
Afsar R NaqviMucosal Immunology Lab, College of Dentistry, University of Illinois at Chicago, Chicago, IL, United States.
University of Illinois Chicago · US

Funding

Human Herpesvirus Impact on Periodontal InflammationR01DE027980 · NIDCR · UNIVERSITY OF ILLINOIS AT CHICAGO · PI NAQVI, AFSAR RAZA · 2018 to 2022
$1.9M
Elucidating the novel regulatory role of long non-coding RNAs in myeloid inflammatory cell differentiation and functionR03DE027147 · NIDCR · UNIVERSITY OF ILLINOIS AT CHICAGO · PI NAQVI, AFSAR RAZA · 2018 to 2019
$320k
NIDCR NIH HHS R01 DE027980NIDCR NIH HHS R03 DE027147
6 · The paper itself

Abstract

Macrophages (Mφ) are long-lived myeloid cells that can polarize towards the proinflammatory M1 or proresolving M2 phenotype to control diverse biological processes such as inflammation, tissue damage, and regeneration. Noncoding RNA are a class of nonprotein-coding transcriptome with numerous interdependent biological roles; however, their functional interaction in the regulation of Mφ polarization and immune responses remain unclear. Here, we show antagonistic relationship between lncRNA (MALAT1) and microRNA (miR-30b) in shaping macrophage polarization and immune functions. MALAT1 expression displays a time-dependent induction during Mφ differentiation and, upon challenge with TLR4 agonist (E. coli LPS). MALAT1 knockdown promoted the expression of M2Mφ markers without affecting M1Mφ markers, suggesting that MALAT1 favors the M1 phenotype by suppressing M2 differentiation. Compared to the control, MALAT1 knockdown resulted in reduced antigen uptake and processing, bacterial phagocytosis, and bactericidal activity, strongly supporting its critical role in regulating innate immune functions in Mφ. Consistent with this, MALAT1 knockdown showed impaired cytokine secretion upon challenge with LPS. Importantly, MALAT1 exhibit an antagonistic expression pattern with all five members of the miR-30 family during M2 Mφ differentiation. Dual-luciferase assays validated a novel sequence on MALAT1 that interacts with miR-30b, a microRNA that promotes the M2 phenotype. Phagocytosis and antigen processing assays unequivocally demonstrated that MALAT1 and miR-30b are functionally antagonistic. Concurrent MALAT1 knockdown and miR-30b overexpression exhibited the most significant attenuation in both assays. In human subjects with periodontal disease and murine model of ligature-induced periodontitis, we observed higher levels of MALAT1, M1Mφ markers and downregulation of miR-30b expression in gingival tissues suggesting a pro-inflammatory function of MALAT1

Indexed as

MicroRNAsRNA, Long NoncodingAnimalsEscherichia coliHumansLipopolysaccharidesMacrophagesMiceLipopolysaccharidesMALAT1 long non-coding RNA, humanMalat1 long non-coding RNA, mouseMicroRNAsMIRN30b microRNA, humanMIRN30b microRNA, mouseRNA, Long NoncodinglncRNA-miRNA interactionlong noncoding RNAmacrophage polarizationMALAT1microRNAmiR-30bmiRNA spongephagocytosis

Identifiers

PMID37860007
PMCPMC10582718
OpenAlexW4387335547

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.