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ArticleMolecular biology reports2024

MiR-146a-5p-enriched exosomes inhibit M1 macrophage activation and inflammatory response by targeting CD80.

Han Zhang, Yifen Wang, Keqing Feng, Qinghui Niu, Yongning Xin, Shiying Xuan, Shousheng Liu

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Article in Molecular biology reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

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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, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. The Role of miRNAs in Parkinson's Disease: A Systematic Review.International journal of molecular sciences · 2025
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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

7 authors.

Han Zhang *Department of Infectious Diseases, Qingdao Municipal Hospital, Qingdao University, 5 Donghaizhong Road, Qingdao, Shandong Province, 266071, China.
Yifen Wang *Department of Infectious Diseases, Qingdao Municipal Hospital, Qingdao University, 5 Donghaizhong Road, Qingdao, Shandong Province, 266071, China.
Keqing FengSchool of Medicine and Pharmacy, Ocean University of China, Qingdao, 266003, China.
Qinghui NiuDepartment of Liver Disease Center, The Affiliated Hospital of Qingdao University, Qingdao, 266071, China.
Yongning XinDepartment of Infectious Diseases, Qingdao Municipal Hospital, Qingdao University, 5 Donghaizhong Road, Qingdao, Shandong Province, 266071, China.
Shiying XuanDepartment of Infectious Diseases, Qingdao Municipal Hospital, Qingdao University, 5 Donghaizhong Road, Qingdao, Shandong Province, 266071, China. xuansydxy@163.com.
Shousheng LiuClinical Research Center, Qingdao Municipal Hospital, 5 Donghaizhong Road, Qingdao, Shandong Province, 266011, China. shoushengliuouc@163.com.

Funding

National Natural Science Foundation of China 32171277Natural Science Foundation of Shandong Province ZR2022QH104
6 · The paper itself

Abstract

backgroundPrevious studies have demonstrated that miR-146a-5p negatively regulated the intrinsic immune and inflammatory responses, whether the miR-146a-5p-enriched exosomes possess the anti-inflammation effect remains unclear. This study aimed to investigate the effect of miR-146a-5p-enriched exosomes on M1 macrophage activation and inflammatory response and the potential molecular mechanism.

methodsGEO database was used to analyze the expression of miR-146a-5p in serum exosomes of MASH patients. MiR-146a-5p levels in primary hepatocytes, macrophages, and serum exosomes of MASH mice were measured. MiR-146a-5p-enriched exosomes were constructed and the effects on M1 macrophages activation and inflammatory factors release were investigated. The target gene of miR-146a-5p was predicted and verified.

resultsSerum exosomal miR-146a-5p level was decreased in MASH patients analyzed by GEO database. The miR-146a-5p levels in primary cultured hepatocytes and macrophages of MASH mice were decreased. Serum exosomal miR-146a-5p level was decreased and negatively correlated with the concentrations of IL-6 in MASH mice. Furthermore, miR-146a-5p-enriched exosomes inhibited the M1 macrophages activation and the expression of pro-inflammatory factors MCP-1, IL-6, and TNF-α. CD80 was predicted as the potential target gene of miR-146a-5p, and the expression of CD80 was regulated by miR-146a-5p. In addition, the inhibitory effect of miR-146a-5p on M1 macrophages activation and inflammatory factors release was restored when CD80 was over-expressed.

conclusionsThis study demonstrated that miR-146a-5p-enriched exosomes can inhibit the M1 macrophages activation and reduce the release of pro-inflammatory factors by targeting CD80.

Indexed as

B7-1 AntigenExosomesInflammationMacrophage ActivationMacrophagesMicroRNAsAnimalsHepatocytesHumansInterleukin-6MaleMiceTumor Necrosis Factor-alphaB7-1 AntigenInterleukin-6MicroRNAsMIRN146 microRNA, humanMirn146 microRNA, mouseTumor Necrosis Factor-alphaCD80ExosomeMetabolic dysfunction-associated steatohepatitisMiR-146a-5p

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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.