Evidence map›Paper›PMID 27844286›Full record

ArticleMolecular neurobiology2017

MFG-E8 Selectively Inhibited Aβ-Induced Microglial M1 Polarization via NF-κB and PI3K-Akt Pathways.

Xiaolei Shi, Xiaoying Cai, Wei Di, Jie Li, Xiaotian Xu, Aiwu Zhang, Weiwei Qi, Zhiming Zhou, Yannan Fang

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.0field-weighted citation impact, top 13% 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, 84 citations in OpenAlex.

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  7. MFG-E8 Ameliorates Nerve Injury-Induced Neuropathic Pain by Regulating Microglial Polarization and Neuroinflammation via Integrin β3/SOCS3/STAT3 Pathway in Mice.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2024
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  17. Efferocytosis in multisystem diseases (Review).Molecular medicine reports · 2022
    Review
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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 4 institutions in 1 country.

Xiaolei ShiDepartment of Neurology, The First Affiliated Hospital, Yijishan Hospital of Wannan Medical College, No. 92 Zheshan West Road, Wuhu, Anhui Province, 241000, People's Republic of China.
Xiaoying CaiGuangdong Key Laboratory for Diagnosis and Treatment of Major Neurological Diseases, Department of Neurology, National Key Clinical Department and Key Discipline of Neurology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong Province, 510080, People's Republic of China.
Wei DiDepartment of Neurology, Shaanxi Provincial People's Hospital, The Third Affiliated Hospital of Xi'an Jiaotong University, Medical College of Xi'an, Xi'an, Shaanxi Province, 710086, People's Republic of China.
Jie LiDepartment of Neurology, Zengcheng People's Hospital, Zengcheng, Guangdong Province, 511300, People's Republic of China.
Xiaotian XuGuangdong Key Laboratory for Diagnosis and Treatment of Major Neurological Diseases, Department of Neurology, National Key Clinical Department and Key Discipline of Neurology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong Province, 510080, People's Republic of China.
Aiwu ZhangGuangdong Key Laboratory for Diagnosis and Treatment of Major Neurological Diseases, Department of Neurology, National Key Clinical Department and Key Discipline of Neurology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong Province, 510080, People's Republic of China.
Weiwei QiGuangdong Key Laboratory for Diagnosis and Treatment of Major Neurological Diseases, Department of Neurology, National Key Clinical Department and Key Discipline of Neurology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong Province, 510080, People's Republic of China.
Zhiming ZhouDepartment of Neurology, The First Affiliated Hospital, Yijishan Hospital of Wannan Medical College, No. 92 Zheshan West Road, Wuhu, Anhui Province, 241000, People's Republic of China.
Yannan FangGuangdong Key Laboratory for Diagnosis and Treatment of Major Neurological Diseases, Department of Neurology, National Key Clinical Department and Key Discipline of Neurology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong Province, 510080, People's Republic of China. fyn2012@126.com.
Sun Yat-sen University · CNFirst Affiliated Hospital of Wannan Medical College · CNShaanxi Provincial People's Hospital · CNTang Hospital · CN

Funding

National Natural Science Fundation of China 81500965Science and Technology Program of Guangzhou 201508020026
6 · The paper itself

Abstract

Activated microglia are classified into two specific states: classically activated (M1) and alternatively activated (M2) subtypes. It is believed that the polarization of M1/M2 phenotype plays an important role in Alzheimer's disease (AD). However, the mechanisms regulating this process remain unclear. Thus, we addressed this question focusing on milk fat globule epidermal growth factor 8 (MFG-E8). MFG-E8 is a unique protein which can bind to microglia and regulate its inflammatory responses. It is speculated that it might play a role in the balance of microglial polarization. In the current study, we used fibril Aβ42 in vitro to stimulate mouse primary microglial cultures and found subsequent M1 marker expression, along with retained M2 marker production. Then, we discovered that MFG-E8 pretreatment reversed the increased trend of M1 markers and the decreased expression of M2 markers, which were induced by Aβ42. Moreover, MFG-E8 effects could be effectively blocked by an MFG-E8 antibody. Further analysis on the signaling pathways showed that NF-κB upregulation and Akt downregulation in microglial cultures were observed after Aβ42 incubation. And the alteration of these pathways could also be reversed by MFG-E8. We then assessed the effects of NF-κB and PI3K-Akt on M1/M2 alteration using their specific inhibitors. Pyrrolidine dithiocarbamate, a NF-κB inhibitor, inhibited M1 marker expression; moreover, LY294002, an Akt inhibitor, enhanced M1 marker expression. Our study indicated the regulatory role of MFG-E8 on microglia M1/M2 alteration for the first time, providing a basis for understanding the potential role of microglia activation in AD.

Indexed as

Amyloid beta-PeptidesAnimalsAnimals, NewbornAntigens, SurfaceCell PolarityCells, CulturedMiceMice, Inbred BALB CMicrogliaMilk ProteinsNF-kappa BPeptide FragmentsPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktSignal TransductionAmyloid beta-Peptidesamyloid beta-protein (1-42)Antigens, SurfaceMfge8 protein, mouseMilk ProteinsNF-kappa BPeptide FragmentsPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktAlzheimer’s diseaseAβ42M1M2MFG-E8Microglia

Identifiers

PMID27844286
OpenAlexW2551162315

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.