Evidence map›Paper›PMID 30060752›Full record

ArticleJournal of neuroinflammation2018

Recombinant CTRP9 administration attenuates neuroinflammation via activating adiponectin receptor 1 after intracerebral hemorrhage in mice.

Lianhua Zhao, Shengpan Chen, Prativa Sherchan, Yan Ding, Wei Zhao, Zaiyu Guo, Jing Yu, Jiping Tang, John H Zhang

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
5.3field-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

42 citing papers in PubMed, 72 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

9 authors at 3 institutions in 2 countries.

Lianhua ZhaoDepartment of Neurology, Tianjin TEDA Hospital, Tianjin, China.
Shengpan ChenDepartment of Physiology and Pharmacology, Loma Linda University, 11041 Campus St, Loma Linda, CA, 92354, USA.
Prativa SherchanDepartment of Physiology and Pharmacology, Loma Linda University, 11041 Campus St, Loma Linda, CA, 92354, USA.
Yan DingDepartment of Physiology and Pharmacology, Loma Linda University, 11041 Campus St, Loma Linda, CA, 92354, USA.
Wei ZhaoDepartment of Neurology, Tianjin TEDA Hospital, Tianjin, China.
Zaiyu GuoDepartment of Neurology, Tianjin TEDA Hospital, Tianjin, China.
Jing YuDepartment of Physiology and Pharmacology, Loma Linda University, 11041 Campus St, Loma Linda, CA, 92354, USA.
Jiping TangDepartment of Physiology and Pharmacology, Loma Linda University, 11041 Campus St, Loma Linda, CA, 92354, USA. jtang@llu.edu.
John H ZhangDepartment of Physiology and Pharmacology, Loma Linda University, 11041 Campus St, Loma Linda, CA, 92354, USA. johnzhang3910@yahoo.com.ORCID http://orcid.org/0000-0002-4319-4285
Loma Linda University · USTEDA International Cardiovascular Hospital · CNCentral South University · CN

Funding

Vascular Biology Core FacilityP01NS082184 · NINDS · LOMA LINDA UNIVERSITY · PI PEARCE, WILLIAM J. · 2014 to 2018
$6.1M
Harnessing Endogenous Neuroprotection Following ICHR01NS091042 · NINDS · LOMA LINDA UNIVERSITY · PI ZHANG, JOHN H · 2016 to 2020
$1.7M
National Institute of Neurological Disorders and Stroke NS082184National Institute of Neurological Disorders and Stroke NS091042NINDS NIH HHS P01 NS082184NINDS NIH HHS R01 NS091042
6 · The paper itself

Abstract

backgroundNeuroinflammation is a crucial factor contributing to neurological injuries after intracerebral hemorrhage (ICH). C1q/TNF-related protein 9 (CTRP9), an agonist of adiponectin receptor 1 (AdipoR1), has recently been shown to reduce inflammatory responses in systemic diseases. The objective of this study was to investigate the protective role of CTRP9 against neuroinflammation after ICH in a mouse model and to explore the contribution of adenosine monophosphate-activated protein kinase (AMPK)/nuclear factor kappa B (NFκB) pathway in AdipoR1-mediated protection.

methodsAdult male CD1 mice (n = 218) were randomly assigned to different groups for the study. ICH was induced via intrastriatal injection of bacterial collagenase. Recombinant CTRP9 (rCTRP9) was administered intranasally at 1 h after ICH. To elucidate the underlying mechanism, AdipoR1 small interfering ribonucleic acid (siRNA) and selective phosphorylated AMPK inhibitor Dorsomorphin were administered prior to rCTRP9 treatment. Brain edema, short- and long-term neurobehavior evaluation, blood glucose level, western blot, and immunofluorescence staining were performed.

resultsEndogenous CTRP9 and AdipoR1 expression was increased and peaked at 24 h after ICH. AdipoR1 was expressed by microglia, neurons, and astrocytes. Administration of rCTRP9 reduced brain edema, improved short- and long-term neurological function, enhanced the expression of AdipoR1 and p-AMPK, and decreased the expression of phosphorylated NFκB and inflammatory cytokines after ICH. The protective effects of rCTRP9 were abolished by administration of AdipoR1 siRNA and Dorsomorphin.

conclusionsOur findings demonstrated that administration of rCTRP9 attenuated neuroinflammation through AdipoR1/AMPK/NFκB signaling pathway after ICH in mice, thereby reducing brain edema and improving neurological function after experimental ICH in mice. Therefore, CTRP9 may provide a potential therapeutic strategy to alleviate neuroinflammation in ICH patients.

Indexed as

AdiponectinAnimalsAnti-Inflammatory AgentsBrain EdemaCerebral HemorrhageDisease Models, AnimalDNA-Binding ProteinsEncephalitisExploratory BehaviorGene Expression RegulationGlycoproteinsMaleMaze LearningMiceNerve Tissue ProteinsNF-kappa BAdiponectinadiponectin receptor 1, mouseAnti-Inflammatory AgentsCTRP9 protein, mouseDNA-Binding ProteinsGlycoproteinsLuzp1 protein, mouseNerve Tissue ProteinsNF-kappa BReceptors, AdiponectinRecombinant ProteinsAdenosine monophosphate-activated protein kinaseAdiponectin receptor 1C1q/TNF-related protein 9Intracerebral hemorrhageNeuroinflammation

Identifiers

PMID30060752
PMCPMC6066941
OpenAlexW2883806546

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.