Evidence map›Paper›PMID 40131162›Full record

ArticleInternational forum of allergy & rhinology2025

MiR-221-3p Attenuates IL-33-Induced Mast Cell Cytokine Expression by Targeting KIT.

Ruowu Liu, Jiao Zhou, Jing Zhou, Feng Liu, Yafeng Liu, Juan Meng, Luo Ba, Hengyi Xiao, Shixi Liu, Nan Zhang and 2 more

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In one paragraph

Article in International forum of allergy & rhinology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

1 citing paper in PubMed.

  1. Review
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.

Ruowu LiuDepartment of Otolaryngology-Head and Neck Surgery, West China Hospital, Sichuan University, Chengdu, China.ORCID 0000-0003-2379-1549
Jiao ZhouDepartment of Medicine and Engineering Interdisciplinary Research Laboratory of Nursing & Materials, West China Hospital, Sichuan University, Chengdu, China.
Jing ZhouDepartment of Otolaryngology-Head and Neck Surgery, West China Hospital, Sichuan University, Chengdu, China.ORCID 0000-0003-2565-9103
Feng LiuDepartment of Otolaryngology-Head and Neck Surgery, West China Hospital, Sichuan University, Chengdu, China.
Yafeng LiuDepartment of Otolaryngology-Head and Neck Surgery, West China Hospital, Sichuan University, Chengdu, China.
Juan MengDepartment of Otolaryngology-Head and Neck Surgery, West China Hospital, Sichuan University, Chengdu, China.
Luo BaDepartment of Otolaryngology, People's Hospital of Tibet Autonomous Region, Lhasa, China.
Hengyi XiaoDepartment of Aging and Geriatric Medicine, National Clinical Research Center for Geriatrics, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.
Shixi LiuDepartment of Otolaryngology-Head and Neck Surgery, West China Hospital, Sichuan University, Chengdu, China.
Nan ZhangDepartment of Otorhinolaryngology-Head and Neck Surgery, University Hospital of Münster, Münster, Germany.
Claus BachertDepartment of Otorhinolaryngology-Head and Neck Surgery, University Hospital of Münster, Münster, Germany.
Jintao DuDepartment of Otolaryngology-Head and Neck Surgery, West China Hospital, Sichuan University, Chengdu, China.ORCID 0000-0001-8552-5508

Funding

National Natural Science Foundation of China 81970858National Natural Science Foundation of China 82160209Natural Science Foundation of Sichuan Province 2024NSFSC1514Postdoctor Research Fund of West China Hospital, Sichuan University 2024HXBH086
6 · The paper itself

Abstract

backgroundMast cells (MCs) are involved in type 2 inflammation in chronic rhinosinusitis with nasal polyps (CRSwNP), which depends on interleukin (IL)-33 stimulation. MiR-221 is reported to be an important regulator of MCs, and miR-221-3p can be expressed in CRSwNP. However, the role of miR-221-3p in CRSwNP is unclear.

methodsEthmoid tissues from control subjects (n = 12) and polyps from patients with CRSwNP (n = 40) were collected. The expression of miR-221-3p and cytokines was detected by real-time quantitative polymerase chain reaction (qPCR). The activation of P65 and ERK was determined by western blotting. The localization of miR-221-3p was detected via in situ hybridization combined with immunofluorescence (IF), and its target was identified via a luciferase reporter system. Human MCs were incubated with IL-33 or stem cell factor. MicroRNA mimics/inhibitor and lentiviral plasmids were used to determine the role of miR-221-3p in MCs.

resultsWe observed increased expression of miR-221-3p in CRSwNP, and localized its expression in MCs. The expression of miR-221-3p was negatively correlated with that of IL-4, IL-5, and IL-13 in CRSwNP. MiR-221-3p can be induced by IL-33 in MCs and plays a negative regulatory role in cytokine expression and signaling pathways in IL-33-induced MC activation. As the direct target of miR-221-3p, the receptor KIT was negatively correlated with miR-221-3p and decreased in CRSwNP. In MCs, KIT is essential for an effective response to IL-33 stimulation. We here demonstrated that miR-221-3p regulates cytokine expression by targeting KIT in IL-33-activated MCs.

conclusionsMiR-221-3p inhibits MC-dependent type 2 inflammatory conditions, rendering it a negative regulator of CRSwNP.

Indexed as

CytokinesInterleukin-33Mast CellsMicroRNAsNasal PolypsProto-Oncogene Proteins c-kitRhinitisSinusitisAdultCells, CulturedChronic DiseaseFemaleHumansMaleMiddle AgedCytokinesIL33 protein, humanInterleukin-33KIT protein, humanMicroRNAsMIR221, humanProto-Oncogene Proteins c-kitCRSwNPIL‐33KITmast cellmiR‐221‐3p

Identifiers

PMID40131162
PMCPMC12315497

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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.