Evidence map›Paper›PMID 33614626›Full record

ArticleFrontiers in cell and developmental biology2020

Inhibition of PDE1-B by Vinpocetine Regulates Microglial Exosomes and Polarization Through Enhancing Autophagic Flux for Neuroprotection Against Ischemic Stroke.

Jiankun Zang, Yousheng Wu, Xuanlin Su, Tianyuan Zhang, Xionglin Tang, Dan Ma, Yufeng Li, Yanfang Liu, Ze'an Weng, Xuanzhuo Liu and 3 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 4% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.

  1. Exosomes in pathogenesis, diagnosis, and therapy of ischemic stroke.Frontiers in bioengineering and biotechnology · 2022
    Pooled it
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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

13 authors at 3 institutions in 2 countries.

Jiankun ZangDepartment of Neurology and Stroke Center, The First Affiliated Hospital, Jinan University, Guangzhou, China.
Yousheng WuDepartment of Neurology and Stroke Center, The First Affiliated Hospital, Jinan University, Guangzhou, China.
Xuanlin SuDepartment of Neurology and Stroke Center, The First Affiliated Hospital, Jinan University, Guangzhou, China.
Tianyuan ZhangDepartment of Neurology and Stroke Center, The First Affiliated Hospital, Jinan University, Guangzhou, China.
Xionglin TangDepartment of Neurology and Stroke Center, The First Affiliated Hospital, Jinan University, Guangzhou, China.
Dan MaSection of Molecular Computational Biology, Department of Biological Sciences, University of Southern California, Los Angeles, CA, United States.
Yufeng LiDepartment of Neurology and Stroke Center, The First Affiliated Hospital, Jinan University, Guangzhou, China.
Yanfang LiuDepartment of Neurology and Stroke Center, The First Affiliated Hospital, Jinan University, Guangzhou, China.
Ze'an WengDepartment of Neurology and Stroke Center, The First Affiliated Hospital, Jinan University, Guangzhou, China.
Xuanzhuo LiuDepartment of Neurology and Stroke Center, The First Affiliated Hospital, Jinan University, Guangzhou, China.
Chi Kwan TsangClinical Neuroscience Institute, The First Affiliated Hospital of Jinan University, Guangzhou, China.
Anding XuDepartment of Neurology and Stroke Center, The First Affiliated Hospital, Jinan University, Guangzhou, China.
Dan LuDepartment of Neurology and Stroke Center, The First Affiliated Hospital, Jinan University, Guangzhou, China.
First Affiliated Hospital of Jinan University · CNAffiliated Hospital of Youjiang Medical University for Nationalities · CNUniversity of Southern California · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Exosomes contribute to cell-cell communications. Emerging evidence has shown that microglial exosomes may play crucial role in regulation of neuronal functions under ischemic conditions. However, the underlying mechanisms of microglia-derived exosome biosynthesis are largely unknown. Herein, we reported that the microglial PDE1-B expression was progressively elevated in the peri-infarct region after focal middle cerebral artery occlusion. By an oxygen-glucose-deprivation (OGD) ischemic model in cells, we found that inhibition of PDE1-B by vinpocetine in the microglial cells promoted M2 and inhibited M1 phenotype. In addition, knockdown or inhibition of PDE1-B significantly enhanced the autophagic flux in BV2 cells, and vinpocetine-mediated suppression of M1 phenotype was dependent on autophagy in ischemic conditions. Co-culture of BV2 cells and neurons revealed that vinpocetine-treated BV2 cells alleviated OGD-induced neuronal damage, and treatment of BV2 cells with 3-MA abolished the observed effects of vinpocetine. We further demonstrated that ischemia and vinpocetine treatment significantly altered microglial exosome biogenesis and release, which could be taken up by recipient neurons and regulated neuronal damage. Finally, we showed that the isolated exosome

Indexed as

autophagyBV2exosomeOGDPDE1vinpocetine

Identifiers

PMID33614626
PMCPMC7889976
OpenAlexW3126831567

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.