Evidence map›Paper›PMID 27241533›Full record

ArticleJournal of cellular and molecular medicine2016

MiR-16 regulates mouse peritoneal macrophage polarization and affects T-cell activation.

Xiaoqin Jia, Xiaomin Li, Yating Shen, Junjun Miao, Hao Liu, Guoli Li, Zhengbing Wang

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

37 citing papers in PubMed, 69 citations in OpenAlex.

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  7. Research progress in effects of microRNAZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2023
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  8. Advances in the Anti-Tumor Activity of Biflavonoids inInternational journal of molecular sciences · 2023
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  15. Article
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  18. Article
  19. MicroRNA-382 Promotes M2-Like MacrophageFrontiers in immunology · 2022
    Article
  20. Article
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 at 1 institution in 1 country.

Xiaoqin JiaDepartment of Pathology, Medical College of Yangzhou University, Yangzhou, Jiangsu, China.
Xiaomin LiDepartment of Pathology, Medical College of Yangzhou University, Yangzhou, Jiangsu, China.
Yating ShenDepartment of Pathology, Medical College of Yangzhou University, Yangzhou, Jiangsu, China.
Junjun MiaoDepartment of Pathology, Medical College of Yangzhou University, Yangzhou, Jiangsu, China.
Hao LiuDepartment of Pathology, Medical College of Yangzhou University, Yangzhou, Jiangsu, China.
Guoli LiDepartment of Pathology, Medical College of Yangzhou University, Yangzhou, Jiangsu, China.
Zhengbing WangDepartment of Gastrointestinal Surgery, Clinical Medical College of Yangzhou University, Yangzhou, Jiangsu, China. wzhb403@163.com.
Yangzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MiR-16 is a tumour suppressor that is down-regulated in certain human cancers. However, little is known on its activity in other cell types. In this study, we examined the biological significance and underlying mechanisms of miR-16 on macrophage polarization and subsequent T-cell activation. Mouse peritoneal macrophages were isolated and induced to undergo either M1 polarization with 100 ng/ml of interferon-γ and 20 ng/ml of lipopolysaccharide, or M2 polarization with 20 ng/ml of interleukin (IL)-4. The identity of polarized macrophages was determined by profiling cell-surface markers by flow cytometry and cytokine production by ELISA. Macrophages were infected with lentivirus-expressing miR-16 to assess the effects of miR-16. Effects on macrophage-T cell interactions were analysed by co-culturing purified CD4(+) T cells with miR-16-expressing peritoneal macrophages, and measuring activation marker CD69 by flow cytometry and cytokine secretion by ELISA. Bioinformatics analysis was applied to search for potential miR-16 targets and understand its underlying mechanisms. MiR-16-induced M1 differentiation of mouse peritoneal macrophages from either the basal M0- or M2-polarized state is indicated by the significant up-regulation of M1 marker CD16/32, repression of M2 marker CD206 and Dectin-1, and increased secretion of M1 cytokine IL-12 and nitric oxide. Consistently, miR-16-expressing macrophages stimulate the activation of purified CD4(+) T cells. Mechanistically, miR-16 significantly down-regulates the expression of PD-L1, a critical immune suppressor that controls macrophage-T cell interaction and T-cell activation. MiR-16 plays an important role in shifting macrophage polarization from M2 to M1 status, and functionally activating CD4(+) T cells. This effect is potentially mediated through the down-regulation of immune suppressor PD-L1.

Indexed as

Cell PolarityAnimalsB7-H1 AntigenBase SequenceCD4-Positive T-LymphocytesCells, CulturedCytokinesLymphocyte ActivationMacrophages, PeritonealMice, Inbred C57BLMicroRNAsPhenotypeT-LymphocytesB7-H1 AntigenCd274 protein, mouseCytokinesMicroRNAsMirn16 microRNA, mouseCD4+ T cellsmacrophage polarizationmiR-16PD-L1

Identifiers

PMID27241533
PMCPMC5020626
OpenAlexW2412240036

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.