Evidence map›Paper›PMID 34376208›Full record

ArticleJournal of neuroinflammation2021

Cathepsin H deficiency decreases hypoxia-ischemia-induced hippocampal atrophy in neonatal mice through attenuated TLR3/IFN-β signaling.

Junjun Ni, Juan Zhao, Xinwen Zhang, Thomas Reinheckel, Vito Turk, Hiroshi Nakanishi

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

14 citing papers in PubMed, 21 citations in OpenAlex.

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  10. Frontiers in pharmacology · 2023
    Article
  11. Regulation of microglia polarization after cerebral ischemia.Frontiers in cellular neuroscience · 2023
    Review
  12. Review
  13. Article
  14. Review
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

6 authors at 5 institutions in 4 countries.

Junjun NiKey Laboratory of Molecular Medicine and Biotherapy, School of Life Science, Beijing Institute of Technology, Beijing, 100081, China. nijunjun@bit.edu.cn.ORCID http://orcid.org/0000-0001-8486-8146
Juan ZhaoKey Laboratory of Molecular Medicine and Biotherapy, School of Life Science, Beijing Institute of Technology, Beijing, 100081, China.
Xinwen ZhangCenter of Implant Dentistry, School of Somatology, China Medical University, Shenyang, 110122, China.
Thomas ReinheckelInstitute of Molecular Medicine and Cell Research, University of Freiburg, 79104, Freiburg, Germany.
Vito TurkDepartment of Biochemistry and Molecular and Structural Biology, J. Stefan Institute, Ljubljana, Slovenia.
Hiroshi NakanishiDepartment of Pharmacology, Faculty of Pharmacy, Yasuda Women's University, Hiroshima, 731-0153, Japan. nakanishi-h@yasuda-u.ac.jp.ORCID https://orcid.org/0000-0003-2610-3203
Beijing Institute of Technology · CNChina Medical University · CNJožef Stefan Institute · SIUniversity of Freiburg · DEYasuda Women's University · JP

Funding

Beijing Natural Science Foundation 7212066Japan Society for the Promotion of Science 18K19650National Natural Science Foundation of China 32070954
6 · The paper itself

Abstract

backgroundCathepsin H (CatH) is a lysosomal cysteine protease with a unique aminopeptidase activity. Its expression level is increased in activated immune cells including dendritic cells, macrophages, and microglia. We have previously reported that CatH deficiency impairs toll-like receptor 3 (TLR3)-mediated activation of interferon regulatory factor 3 (IRF3), and the subsequent secretion of interferon (IFN)-β from dendritic cells. Furthermore, there is increasing evidence that IFN-β secreted from microglia/macrophages has neuroprotective effects. These observations prompted further investigation into the effects of CatH deficiency on neuropathological changes.

methodsIn this study, neuropathological changes were examined using histochemical staining (both hematoxylin-eosin (H&E) and Nissl) of the hippocampus of wild-type (WT) and CatH-deficient (CatH

resultsWT mice displayed severe atrophy in association with neuronal death and moderate astrogliosis in the hippocampus following neonatal HI. Somewhat surprisingly, CatH

conclusionThese observations suggest that CatH plays a critical role in the proteolytic maturation and stabilization of TLR3, which is necessary for IFN-β production. Therefore, impaired TLR3/IFN-β signaling resulting from CatH deficiency may induce microglial cell death after activation and astrogliosis/glial scar formation in the hippocampus following HI injury, leading to suppression of hippocampal atrophy.

Indexed as

AnimalsAtrophyCathepsin HCell DeathHippocampusHypoxia-Ischemia, BrainInterferon-betaMiceMice, KnockoutMicrogliaSignal TransductionToll-Like Receptor 3Cathepsin HInterferon-betaToll-Like Receptor 3AstrocyteCathepsin HInterferon-βMicroglia/Macrophages

Identifiers

PMID34376208
PMCPMC8353845
OpenAlexW3188488486

What OpenQuestion holds

Textmetadata
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.