Evidence map›Paper›PMID 29275848›Full record

ArticleMolecular therapy : the journal of the American Society of Gene Therapy2018

miR-23b Suppresses Leukocyte Migration and Pathogenesis of Experimental Autoimmune Encephalomyelitis by Targeting CCL7.

Yuan Zhang, Juan-Juan Han, Xiao-Yan Liang, Li Zhao, Fei Zhang, Javad Rasouli, Zhe-Zhi Wang, Guang-Xian Zhang, Xing Li

Open access · bronzeAbstract read
In one paragraph

Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

45 citing papers in PubMed, 67 citations in OpenAlex.

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  20. CD4Journal of neuroinflammation · 2022
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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

9 authors at 2 institutions in 2 countries.

Yuan ZhangKey Laboratory of the Ministry of Education for Medicinal Resources and Natural Pharmaceutical Chemistry, National Engineering Laboratory for Resource Development of Endangered Crude Drugs in Northwest China, College of Life Sciences, Shaanxi Normal University, Xi'an 710119, China; Department of Neurology, Thomas Jefferson University, Philadelphia, PA 19107, USA.
Juan-Juan HanKey Laboratory of the Ministry of Education for Medicinal Resources and Natural Pharmaceutical Chemistry, National Engineering Laboratory for Resource Development of Endangered Crude Drugs in Northwest China, College of Life Sciences, Shaanxi Normal University, Xi'an 710119, China.
Xiao-Yan LiangKey Laboratory of the Ministry of Education for Medicinal Resources and Natural Pharmaceutical Chemistry, National Engineering Laboratory for Resource Development of Endangered Crude Drugs in Northwest China, College of Life Sciences, Shaanxi Normal University, Xi'an 710119, China.
Li ZhaoKey Laboratory of the Ministry of Education for Medicinal Resources and Natural Pharmaceutical Chemistry, National Engineering Laboratory for Resource Development of Endangered Crude Drugs in Northwest China, College of Life Sciences, Shaanxi Normal University, Xi'an 710119, China.
Fei ZhangKey Laboratory of the Ministry of Education for Medicinal Resources and Natural Pharmaceutical Chemistry, National Engineering Laboratory for Resource Development of Endangered Crude Drugs in Northwest China, College of Life Sciences, Shaanxi Normal University, Xi'an 710119, China.
Javad RasouliDepartment of Neurology, Thomas Jefferson University, Philadelphia, PA 19107, USA.
Zhe-Zhi WangKey Laboratory of the Ministry of Education for Medicinal Resources and Natural Pharmaceutical Chemistry, National Engineering Laboratory for Resource Development of Endangered Crude Drugs in Northwest China, College of Life Sciences, Shaanxi Normal University, Xi'an 710119, China.
Guang-Xian ZhangDepartment of Neurology, Thomas Jefferson University, Philadelphia, PA 19107, USA. Electronic address: guang-xian.zhang@jefferson.edu.
Xing LiKey Laboratory of the Ministry of Education for Medicinal Resources and Natural Pharmaceutical Chemistry, National Engineering Laboratory for Resource Development of Endangered Crude Drugs in Northwest China, College of Life Sciences, Shaanxi Normal University, Xi'an 710119, China; Department of Neurology, Thomas Jefferson University, Philadelphia, PA 19107, USA. Electronic address: xingli_xian@126.com.
Shaanxi Normal University · CNThomas Jefferson University · US

Funding

NSCs produce a triply effective cocktail in the CNS for MS/EAE therapyR01NS075260 · NINDS · THOMAS JEFFERSON UNIVERSITY · PI ZHANG, GUANG-XIAN · 2012 to 2016
$1.5M
NINDS NIH HHS R01 NS075260
6 · The paper itself

Abstract

MicroRNAs (miRNAs) are small, non-coding RNAs involved in immune response regulation. Specific miRNAs have been linked to the development of various autoimmune diseases; however, their contribution to the modulation of CNS-directed cellular infiltration remains unclear. In this study, we found that miR-23b, in addition to its reported functions in the suppression of IL-17-associated autoimmune inflammation, halted the progression of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS), by directly inhibiting the migration of pathogenic leukocytes to the CNS. We demonstrated that miR-23b was specifically decreased during the acute phase of EAE and that overexpression of miR-23b resulted in a defect in leukocyte migration and strong resistance to EAE. Furthermore, we found that miR-23b suppressed leukocyte migration of EAE by targeting CCL7, a chemokine that attracts monocytes during inflammation and metastasis. Finally, in the adoptive transfer model, miR-23b reduced the severity of EAE by inhibiting the migration of pathogenic T cells to the CNS rather than diminishing the encephalitogenesis of T cells. Taken together, our results characterize a novel aspect of miR-23b function in leukocyte migration, and they identify miR-23b as a potential therapeutic target in the amelioration of MS and likely other autoimmune diseases.

Indexed as

3' Untranslated RegionsAnimalsChemokine CCL7Chemotaxis, LeukocyteEncephalomyelitis, Autoimmune, ExperimentalFemaleGene Expression RegulationImmunophenotypingLeukocytesLymphocyte ActivationMiceMicroRNAsRNA InterferenceT-Lymphocytes3' Untranslated RegionsChemokine CCL7MicroRNAsMirn23b microRNA, mouseCCL7cellular migrationmicroRNAmiR-23bmultiple sclerosis

Identifiers

PMID29275848
PMCPMC5835026
OpenAlexW2768945903

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.