Evidence map›Paper›PMID 31811815›Full record

ArticleAging2019

Melatonin protects blood-brain barrier integrity and permeability by inhibiting matrix metalloproteinase-9 via the NOTCH3/NF-κB pathway.

Weiwei Qin, Jing Li, Rongjia Zhu, Suhua Gao, Junfen Fan, Mingrong Xia, Robert Chunhua Zhao, Jiewen Zhang

Open access · greenAbstract read
In one paragraph

Article in Aging, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 1 pooled it
5.7field-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

67 citing papers in PubMed, 1 synthesis or guideline pooled it, 117 citations in OpenAlex.

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7 more citing papers are in PubMed but not listed here.

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

8 authors at 3 institutions in 1 country.

Weiwei QinDepartment of Neurology, State Key Clinical Specialty of the Ministry of Health for Neurology, Henan Provincial People's Hospital, School of Clinical Medicine, Henan University, Zhengzhou, Henan, China.
Jing LiInstitute of Basic Medical Sciences Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Center of Excellence in Tissue Engineering Chinese Academy of Medical Sciences, Beijing Key Laboratory (No. BZO381), Beijing 100005, China.
Rongjia ZhuInstitute of Basic Medical Sciences Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Center of Excellence in Tissue Engineering Chinese Academy of Medical Sciences, Beijing Key Laboratory (No. BZO381), Beijing 100005, China.
Suhua GaoDepartment of Scientific Research and Discipline Construction, Henan Provincial People's Hospital, Zhengzhou, Henan, China.
Junfen FanInstitute of Basic Medical Sciences Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Center of Excellence in Tissue Engineering Chinese Academy of Medical Sciences, Beijing Key Laboratory (No. BZO381), Beijing 100005, China.
Mingrong XiaDepartment of Neurology, State Key Clinical Specialty of the Ministry of Health for Neurology, Henan Provincial People's Hospital, School of Clinical Medicine, Henan University, Zhengzhou, Henan, China.
Robert Chunhua ZhaoInstitute of Basic Medical Sciences Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Center of Excellence in Tissue Engineering Chinese Academy of Medical Sciences, Beijing Key Laboratory (No. BZO381), Beijing 100005, China.
Jiewen ZhangDepartment of Neurology, State Key Clinical Specialty of the Ministry of Health for Neurology, Henan Provincial People's Hospital, School of Clinical Medicine, Henan University, Zhengzhou, Henan, China.
Chinese Academy of Medical Sciences & Peking Union Medical College · CNHenan Provincial People's Hospital · CNHenan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The pathophysiological mechanism of white matter hyperintensities of cerebral small vessel disease (CSVD) includes an impaired blood-brain barrier (BBB) with increased permeability. Neuroinflammation likely contributes to the disruption of the BBB in CSVD. Therefore, understanding the molecular mechanism of how neuroinflammation causes BBB damage is essential to preventing BBB disruption in CSVD. Matrix metalloproteinase 9 (MMP-9) contributes to BBB damage in neuroinflammatory diseases. In this study, we observed that interleukin-1β (IL-1β)-induced MMP-9 secretion in pericytes increased BBB permeability to sodium fluorescein (Na-F) by damaging the disruption of VE-cadherin, occludin, claudin-5, and zonula occludin-1 (ZO-1). Melatonin reduced BBB permeability to Na-F and inhibited the disruption of the adherens and tight junction proteins. Melatonin also downregulated

Indexed as

Adherens JunctionsAstrocytesBlood-Brain BarrierCells, CulturedCoculture TechniquesEndothelial CellsGene Expression RegulationHumansMatrix Metalloproteinase 9MelatoninNF-kappa BPericytesPermeabilityReceptor, Notch3RNA, MessengerTight Junction ProteinsMatrix Metalloproteinase 9MelatoninMMP9 protein, humanNF-kappa BNOTCH3 protein, humanReceptor, Notch3RNA, MessengerTight Junction Proteinsblood-brain barriermatrix metalloproteinase-9NOTCH3nuclear factor κBpericytes

Identifiers

PMID31811815
PMCPMC6932927
OpenAlexW2992544017

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.