Evidence map›Paper›PMID 31779639›Full record

ArticleJournal of neuroinflammation2019

DHEA Attenuates Microglial Activation via Induction of JMJD3 in Experimental Subarachnoid Haemorrhage.

Tao Tao, Guang-Jie Liu, Xuan Shi, Yan Zhou, Yue Lu, Yong-Yue Gao, Xiang-Sheng Zhang, Han Wang, Ling-Yun Wu, Chun-Lei Chen and 3 more

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2019. 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
3.0field-weighted citation impact, top 8% 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, 53 citations in OpenAlex.

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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 1 country.

Tao TaoDepartment of Neurosurgery, Nanjing Drum Tower Hospital Clinical College of Nanjing Medical University, Nanjing, 210008, Jiangsu, China.
Guang-Jie LiuDepartment of Neurosurgery, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Nanjing, 210008, Jiangsu, China.
Xuan ShiDepartment of Neurology, Jinling Hospital, Nanjing Medical University, Nanjing, China.
Yan ZhouDepartment of Neurosurgery, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Nanjing, 210008, Jiangsu, China.
Yue LuDepartment of Neurosurgery, Nanjing Drum Tower Hospital Clinical College of Nanjing Medical University, Nanjing, 210008, Jiangsu, China.
Yong-Yue GaoDepartment of Neurosurgery, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Nanjing, 210008, Jiangsu, China.
Xiang-Sheng ZhangDepartment of Neurosurgery, Beijing Friendship Hospital, Capital Medical University, Beijing, 100032, China.
Han WangDepartment of Neurosurgery, Nanjing Drum Tower Hospital Clinical College of Nanjing Medical University, Nanjing, 210008, Jiangsu, China.
Ling-Yun WuDepartment of Neurosurgery, Nanjing Drum Tower Hospital Clinical College of Nanjing Medical University, Nanjing, 210008, Jiangsu, China.
Chun-Lei ChenDepartment of Neurosurgery, Nanjing Drum Tower Hospital Clinical College of Nanjing Medical University, Nanjing, 210008, Jiangsu, China.
Zong ZhuangDepartment of Neurosurgery, Nanjing Drum Tower Hospital Clinical College of Nanjing Medical University, Nanjing, 210008, Jiangsu, China.
Wei LiDepartment of Neurosurgery, Nanjing Drum Tower Hospital Clinical College of Nanjing Medical University, Nanjing, 210008, Jiangsu, China. lwxzlw@126.com.
Chun-Hua HangDepartment of Neurosurgery, Nanjing Drum Tower Hospital Clinical College of Nanjing Medical University, Nanjing, 210008, Jiangsu, China. hang_neurosurgery@163.com.ORCID http://orcid.org/0000-0001-8687-7599
Nanjing Drum Tower Hospital · CNCapital Medical University · CNNanjing General Hospital of Nanjing Military Command · CN

Funding

Fundamental Research Funds for the Central Universities 021414380361Key Project supported by Medical Science and Technology development Foundation,Nanjing Department of Health JQX18001National Natural Science Foundation of China 81771291National Natural Science Foundation of China 81801166National Natural Science Foundation of China 81870922National Natural Science Foundation of China 81901203National Natural Science Foundation of China 81971127
6 · The paper itself

Abstract

backgroundMicroglia are resident immune cells in the central nervous system and central to the innate immune system. Excessive activation of microglia after subarachnoid haemorrhage (SAH) contributes greatly to early brain injury, which is responsible for poor outcomes. Dehydroepiandrosterone (DHEA), a steroid hormone enriched in the brain, has recently been found to regulate microglial activation. The purpose of this study was to address the role of DHEA in SAH.

methodsWe used in vivo models of endovascular perforation and in vitro models of haemoglobin exposure to illustrate the effects of DHEA on microglia in SAH.

resultsIn experimental SAH mice, exogenous DHEA administration increased DHEA levels in the brain and modulated microglial activation. Ameliorated neuronal damage and improved neurological outcomes were also observed in the SAH mice pretreated with DHEA, suggesting neuronal protective effects of DHEA. In cultured microglia, DHEA elevated the mRNA and protein levels of Jumonji d3 (JMJD3, histone 3 demethylase) after haemoglobin exposure, downregulated the H3K27me3 level, and inhibited the transcription of proinflammatory genes. The devastating proinflammatory microglia-mediated effects on primary neurons were also attenuated by DHEA; however, specific inhibition of JMJD3 abolished the protective effects of DHEA. We next verified that DHEA-induced JMJD3 expression, at least in part, through the tropomyosin-related kinase A (TrkA)/Akt signalling pathway.

conclusionsDHEA has a neuroprotective effect after SAH. Moreover, DHEA increases microglial JMJD3 expression to regulate proinflammatory/anti-inflammatory microglial activation after haemoglobin exposure, thereby suppressing inflammation.

Indexed as

AnimalsBrainCells, CulturedDehydroepiandrosteroneDisease Models, AnimalJumonji Domain-Containing Histone DemethylasesMaleMiceMicrogliaNeuronsNeuroprotective AgentsSignal TransductionSubarachnoid HemorrhageDehydroepiandrosteroneJumonji Domain-Containing Histone DemethylasesKdm6b protein, mouseNeuroprotective AgentsDehydroepiandrosteroneInflammationJMJD3MicrogliaSubarachnoid haemorrhage

Identifiers

PMID31779639
PMCPMC6883548
OpenAlexW2991013813

What OpenQuestion holds

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LicenceCC BY
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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.